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        <title>CNS Neuroscience and Therapeutics via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'CNS Neuroscience and Therapeutics' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=CNS+Neuroscience+and+Therapeutics&t=CNS+Neuroscience+and+Therapeutics&s=Search&f=source]]></link>
        <lastBuildDate>Tue, 07 Feb 2012 07:05:40 +0100</lastBuildDate>
        <item>
            <title>Genetic Polymorphism of NAT2 Metabolizing Enzymes on Phenytoin Pharmacokinetics in Indian Epileptic Patients Developing Toxicity.</title>
            <link>http://www.medworm.com/index.php?rid=5639604&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22268821%26dopt%3DAbstract</link>
            <description>Conclusion: Our findings suggest that the NAT2*5A genetic polymorphisms plays a significant role in the steady-state concentrations of phenytoin and thereby have impact on toxicity in epileptic patients.
    PMID: 22268821 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
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            <pubDate>Tue, 24 Jan 2012 05:00:00 +0100</pubDate>
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            <title>Classifying Ischemic Stroke, from TOAST to CISS.</title>
            <link>http://www.medworm.com/index.php?rid=5639600&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22268862%26dopt%3DAbstract</link>
            <description>Authors: Chen PH, Gao S, Wang YJ, Xu AD, Li YS, Wang D
    Abstract
    SUMMARY  Ischemic stroke classification is critical in conducting basic research and clinical practice. A precise analysis of stroke subtypes requires the integration of clinical features, findings from diagnostic tests, and knowledge about potential etiologic factors by competent diagnostic investigators. We performed a literature review of the published stroke classification systems and examined each for its benefits and limitations in the evaluation of the stroke etiology. Two major approaches to etiologic classifications of ischemic stroke are currently being used: the causative and phenotypic subtyping. The most widely used causative system is the Trial of Org 10172 in acute stroke treatment (TOAST) classificati...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
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            <pubDate>Tue, 24 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Research highlights.</title>
            <link>http://www.medworm.com/index.php?rid=5639599&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22280155%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22280155 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5639599</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>The new editorial team at CNS neuroscience and therapeutics.</title>
            <link>http://www.medworm.com/index.php?rid=5639598&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22280156%26dopt%3DAbstract</link>
            <description>Authors: Su DF
    PMID: 22280156 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5639598</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5639598</guid>        </item>
        <item>
            <title>d-Serine Regulates Proliferation and Neuronal Differentiation of Neural Stem Cells from Postnatal Mouse Forebrain.</title>
            <link>http://www.medworm.com/index.php?rid=5639597&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22280157%26dopt%3DAbstract</link>
            <description>Conclusions: Our findings demonstrate for the first time that NSCs can synthesize d-serine and, thereby, promote themselves proliferation and neuronal differentiation, which may afford a novel therapeutic strategy for the neurological disorders that require nerve cell replenishment, such as neurodegenerative diseases and stroke.
    PMID: 22280157 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
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            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>A Neuroprotective Mechanism of YGY-E in Cerebral Ischemic Injury in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5639596&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22280158%26dopt%3DAbstract</link>
            <description>Conclusions: Our findings indicate that YGY-E's neuroprotective effects may be because of its inhibition of neuronal apoptosis by increasing Bcl-2 expression.
    PMID: 22280158 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
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            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Situational rumination: a method for minimizing retrospective reporting bias.</title>
            <link>http://www.medworm.com/index.php?rid=5639595&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22280159%26dopt%3DAbstract</link>
            <description>Authors: McMurrich SL, Johnson SL, Peckham AD
    PMID: 22280159 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
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            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Effect of edaravone on aβ(1-40)  induced enhancement of voltage-gated calcium channel current.</title>
            <link>http://www.medworm.com/index.php?rid=5639594&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22280160%26dopt%3DAbstract</link>
            <description>Effect of edaravone on aβ(1-40) induced enhancement of voltage-gated calcium channel current.
    CNS Neurosci Ther. 2012 Jan;18(1):89-90
    Authors: He F, Luan P, He R, Zhao ZY, Sun ZQ, Che FY, Xing YG, Liu J
    PMID: 22280160 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
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            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5639594</guid>        </item>
        <item>
            <title>Clots and blots: a stroke of good fortune in identifying protein changes in cerebral accidents.</title>
            <link>http://www.medworm.com/index.php?rid=5456283&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22117797%26dopt%3DAbstract</link>
            <description>Authors: Laher I
    PMID: 22117797 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5456283</comments>
            <pubDate>Wed, 30 Nov 2011 11:55:28 +0100</pubDate>
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        <item>
            <title>Toward a unifying hypothesis in the development of Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=5456282&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22117798%26dopt%3DAbstract</link>
            <description>Authors: Balin B, Abrams JT, Schrogie J
    PMID: 22117798 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5456282</comments>
            <pubDate>Wed, 30 Nov 2011 11:55:20 +0100</pubDate>
            <guid isPermaLink="false">5456282</guid>        </item>
        <item>
            <title>Increased oxidative stress is responsible for severer cerebral infarction in stroke-prone spontaneously hypertensive rats.</title>
            <link>http://www.medworm.com/index.php?rid=5456281&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22117799%26dopt%3DAbstract</link>
            <description>Conclusions: Our findings indicate that oxidative stress plays an important role in the pathogenesis of cerebral ischemia.
    PMID: 22117799 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5456281</comments>
            <pubDate>Wed, 30 Nov 2011 11:55:11 +0100</pubDate>
            <guid isPermaLink="false">5456281</guid>        </item>
        <item>
            <title>Chronic, recurrent headache in cerebral venous sinus thrombosis.</title>
            <link>http://www.medworm.com/index.php?rid=5456280&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22117800%26dopt%3DAbstract</link>
            <description>Authors: Zhang SQ, Ma XL, Guan YT, Zheng HM
    PMID: 22117800 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5456280</comments>
            <pubDate>Wed, 30 Nov 2011 11:55:03 +0100</pubDate>
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        <item>
            <title>A new index to predict the incidence of cerebral infarction.</title>
            <link>http://www.medworm.com/index.php?rid=5456279&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22117801%26dopt%3DAbstract</link>
            <description>Authors: Hao CN, Huang ZH, Shi YQ, Lu W, Duan JL
    PMID: 22117801 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5456279</comments>
            <pubDate>Wed, 30 Nov 2011 11:54:54 +0100</pubDate>
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        <item>
            <title>Cerebral artery remodeling in stroke-prone spontaneously hypertensive rats.</title>
            <link>http://www.medworm.com/index.php?rid=5456278&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22117802%26dopt%3DAbstract</link>
            <description>Authors: Yang C, Zhang X, Song SW, Yu JG, Cai GJ
    PMID: 22117802 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5456278</comments>
            <pubDate>Wed, 30 Nov 2011 11:54:46 +0100</pubDate>
            <guid isPermaLink="false">5456278</guid>        </item>
        <item>
            <title>Role of Intracranial Microaneurysm in the Pathogenesis of Stroke in SHR-SP.</title>
            <link>http://www.medworm.com/index.php?rid=5456277&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22117803%26dopt%3DAbstract</link>
            <description>Authors: Yang C, Yu JG, Liu JG, Cai GJ, Su DF
    PMID: 22117803 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5456277</comments>
            <pubDate>Wed, 30 Nov 2011 11:54:37 +0100</pubDate>
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        <item>
            <title>Verification of motion sickness index in mice.</title>
            <link>http://www.medworm.com/index.php?rid=5456276&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22117804%26dopt%3DAbstract</link>
            <description>Authors: Wei X, Wang ZB, Zhang LC, Liu WY, Su DF, Li L
    PMID: 22117804 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5456276</comments>
            <pubDate>Wed, 30 Nov 2011 11:54:29 +0100</pubDate>
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            <title>An Association Analysis between 5-HTTLPR Polymorphism and Obsessive-Compulsive Disorder, Tourette Syndrome in a Chinese Han Population.</title>
            <link>http://www.medworm.com/index.php?rid=5456275&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22117805%26dopt%3DAbstract</link>
            <description>Authors: Liu SG, Zhang XH, Yin YY, Wang MJ, Che FY, Ma X
    PMID: 22117805 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5456275</comments>
            <pubDate>Wed, 30 Nov 2011 11:54:20 +0100</pubDate>
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        <item>
            <title>Potentiation of D-Serine Involves Degeneration of Dopaminergic Neurons in MPTP/p Mouse Model of Parkinson's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=5456274&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22117806%26dopt%3DAbstract</link>
            <description>Authors: Lu M, Fan Y, Tang M, Qian X, Ding J, Hu G
    PMID: 22117806 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5456274</comments>
            <pubDate>Wed, 30 Nov 2011 11:54:10 +0100</pubDate>
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            <title>A Novel, Nonbinary Evaluation of Success and Failure Reveals Bupropion Efficacy Versus Methamphetamine Dependence: Reanalysis of a Multisite Trial.</title>
            <link>http://www.medworm.com/index.php?rid=5420161&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22070720%26dopt%3DAbstract</link>
            <description>Authors: McCann DJ, Li SH
    Abstract
    A multisite, double-blind, placebo-controlled trial of bupropion for methamphetamine dependence was reanalyzed using a novel, nonbinary method of evaluating success and failure. The original analysis focused on a group response endpoint (the change in percentage of participants with methamphetamine-free urines each week over the course of the trial) and no significant bupropion effect was observed in the total population of study participants. In this reanalysis, individual participants were regarded as treatment success if they achieved multiple weeks of abstinence lasting through the end of the study, and their degree of success was quantified by calculating the number of beyond-threshold weeks of success (NOBWOS). Thus, setting the threshold at...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
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            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
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            <title>A Double-Blind Randomized Controlled Trial To Study the Efficacy of Topiramate in a Civilian Sample of PTSD.</title>
            <link>http://www.medworm.com/index.php?rid=5297135&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21554564%26dopt%3DAbstract</link>
            <description>Conclusion: Topiramate was effective in improving reexperiencing and avoidance/numbing symptom clusters in patients with PTSD. This study supports the use of anticonvulsants for the improvement of symptoms of PTSD.
    PMID: 21554564 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5297135</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
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            <title>Acupuncture for depression: a critique of the evidence base.</title>
            <link>http://www.medworm.com/index.php?rid=5280141&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21091639%26dopt%3DAbstract</link>
            <description>Conclusion: Uncertainty remains about the value of acupuncture care, as it is routinely practiced in the West, and this uncertainty has not been resolved by trials to date. Existing evaluations may however be useful for guiding decisions about the value of specific techniques for patients with depression.
    PMID: 21091639 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280141</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
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            <title>Agomelatine: protecting the CNS from the effects of stress.</title>
            <link>http://www.medworm.com/index.php?rid=5280140&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951364%26dopt%3DAbstract</link>
            <description>Authors: Maccari S, Nicoletti F
    PMID: 21951364 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280140</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
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            <title>Hypothermia reduces brain edema, spontaneous recurrent seizure attack, and learning memory deficits in the kainic Acid treated rats.</title>
            <link>http://www.medworm.com/index.php?rid=5280139&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951365%26dopt%3DAbstract</link>
            <description>Conclusions: Hypothermia treatment immediately after SE not only exhibited protective effects against the chronic spontaneous recurrent convulsant seizures but also improved cognitive function. These antiepileptogenic properties of hypothermia may be related to its attenuating effect on brain edema induced by SE. They therefore suggest that brain edema may be involved in the progress of epileptogenesis.
    PMID: 21951365 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
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            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
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        <item>
            <title>Deficiency of NG2(+)  Cells Contributes to the Susceptibility of Stroke-Prone Spontaneously Hypertensive Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5280138&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951366%26dopt%3DAbstract</link>
            <description>Conclusion: The decline of NG2(+) cells may cause demyelination and contribute to the susceptibility of SHR-SP to ischemic brain injury.
    PMID: 21951366 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280138</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5280138</guid>        </item>
        <item>
            <title>Possible role of glia in cognitive impairment in schizophrenia.</title>
            <link>http://www.medworm.com/index.php?rid=5280137&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951367%26dopt%3DAbstract</link>
            <description>Authors: Mitterauer BJ
    Abstract
    Cognitive impairment is a core disorder of the schizophrenia syndrome. Based on glial-neuronal interactions, a pathophysiological model is proposed that could be explanatory for cognitive impairment in schizophrenia. The model consists of three main hypotheses concerning the pathophysiology in tripartite synapses, oligodendrocyte-axonic interactions, and in the glial networks (astrocytic syncytium). In tripartite synapses nonfunctional astrocytic receptors may cause an unconstrained synaptic information flux, since they cannot be occupied by neurotransmitters (NTs). Therefore, a generalization of information processing may occur in the brain causing hallucinations, delusions, and thought disorder. If the oligodendrocyte-axonic system decomposes, the ...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280137</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5280137</guid>        </item>
        <item>
            <title>Effects of Cholinesterase Inhibitors in Parkinson's Disease Dementia: A Review of Clinical Data.</title>
            <link>http://www.medworm.com/index.php?rid=5280136&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951368%26dopt%3DAbstract</link>
            <description>Conclusions: Taken together, these studies suggest that ChEIs are efficacious in the treatment of PDD.
    PMID: 21951368 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280136</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5280136</guid>        </item>
        <item>
            <title>Acute drug administration in epilepsy: a review.</title>
            <link>http://www.medworm.com/index.php?rid=5280135&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951369%26dopt%3DAbstract</link>
            <description>Conclusions: The best evidence for the efficacy of ADA exists in febrile and nonfebrile childhood seizures, whereas the evidence in catamenial epilepsy is weak. Prevention of clusters is a well-proven principle but its application has been little studied. Prevention of imminent seizures predicted by well-established triggers, defined risk factors, or premonitory minor seizure activity seems to be at the same time the most intelligent and the least investigated application of ADA and would deserve to be better studied.
    PMID: 21951369 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280135</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5280135</guid>        </item>
        <item>
            <title>The use of antidepressants for headache prophylaxis.</title>
            <link>http://www.medworm.com/index.php?rid=5280134&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951370%26dopt%3DAbstract</link>
            <description>Authors: Smitherman TA, Walters AB, Maizels M, Penzien DB
    Abstract
    The focus of this review is on the efficacy of antidepressants as preventive treatments for migraine and chronic tension-type headache (TTH). Pharmacologic prophylaxis may be indicated for patients with frequent headaches, who respond insufficiently to acute therapies, or for whom medication overuse is a concern. The well-documented efficacy of the tricyclic antidepressant amitriptyline, both for migraine and chronic TTH, has been followed by widespread use of other antidepressants for headache prophylaxis. Although antidepressants in general share comparable efficacy for the treatment of depressive disorders, their efficacy as headache preventives varies widely. Evidence supporting use of the selective serotonin re...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280134</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5280134</guid>        </item>
        <item>
            <title>Neuropsychiatric adverse effects of centrally acting antiobesity drugs.</title>
            <link>http://www.medworm.com/index.php?rid=5280133&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951371%26dopt%3DAbstract</link>
            <description>Conclusion: These findings highlight the need to assess neuropsychiatric adverse events comprehensively using sensitive and validated methods early in the clinical development of candidate antiobesity drugs with a central mechanism of action.
    PMID: 21951371 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280133</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5280133</guid>        </item>
        <item>
            <title>The genetics of white matter lesions.</title>
            <link>http://www.medworm.com/index.php?rid=5280132&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951372%26dopt%3DAbstract</link>
            <description>Authors: Assareh A, Mather KA, Schofield PR, Kwok JB, Sachdev PS
    Abstract
    White matter lesions (WMLs), commonly seen as hyperintensities on T2-weighted MRI scans of healthy elderly individuals, are considered to be related to small vessel disease in the brain, and are often associated with subtle cognitive and functional impairments. WMLs also show a strong correlation with a wide range of neurodegenerative and neuropsychiatric disorders. Although a number of vascular risk factors for WMLs have been identified, genetic factors are also important with twin and family studies reporting high heritability. Mutations in several genes have been described that lead to monogenic disorders manifesting WMLs, such as Fabry disease and CADASIL. Because most individuals with WMLs do not have Me...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280132</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5280132</guid>        </item>
        <item>
            <title>From hypertension to stroke: mechanisms and potential prevention strategies.</title>
            <link>http://www.medworm.com/index.php?rid=5280131&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951373%26dopt%3DAbstract</link>
            <description>Authors: Yu JG, Zhou RR, Cai GJ
    Abstract
    Stroke is a major cause of disability and death worldwide. Prevention aimed at risk factors of stroke is the most effective strategy to curb the stroke pandemic. Hypertension is one of the most important risk factors for stroke. Despite the substantial evidence of the benefits of lowering blood pressure, conventional treatment does not normalize the burden of major cardiovascular events in patients with hypertension. Fully understanding the factors involved in the hypertension-induced stroke helps to develop new strategies for stroke prevention. Antihypertensive therapies selected should have positive blood pressure-independent effects on stroke risk. This review summarizes the factors involved in the hypertension-induced stroke, such as oxi...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5280131</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5280131</guid>        </item>
        <item>
            <title>Schizophrenia diagnosis and treatment.</title>
            <link>http://www.medworm.com/index.php?rid=4643389&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21401910%26dopt%3DAbstract</link>
            <description>Authors: Seeman P
    
    PMID: 21401910 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4643389</comments>
            <pubDate>Tue, 29 Mar 2011 10:15:12 +0100</pubDate>
            <guid isPermaLink="false">4643389</guid>        </item>
        <item>
            <title>Treatment strategies for dosing the second generation antipsychotics.</title>
            <link>http://www.medworm.com/index.php?rid=4643388&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21401911%26dopt%3DAbstract</link>
            <description>Conclusion: The second generation antipsychotics have many clinical applications in psychiatric practice. This article serves to review this and also suggests ways clinicians may optimize treatment based upon patient diagnosis and utilizing appropriate dosing of each individual second generation antipsychotic.
    PMID: 21401911 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4643388</comments>
            <pubDate>Tue, 29 Mar 2011 10:15:07 +0100</pubDate>
            <guid isPermaLink="false">4643388</guid>        </item>
        <item>
            <title>Should we listen to people affected by dementia?</title>
            <link>http://www.medworm.com/index.php?rid=4406539&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21235731%26dopt%3DAbstract</link>
            <description>Authors: Rockwood K
    
    PMID: 21235731 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4406539</comments>
            <pubDate>Fri, 28 Jan 2011 14:15:06 +0100</pubDate>
            <guid isPermaLink="false">4406539</guid>        </item>
        <item>
            <title>Neuropsychiatric Aspects of Schizophrenia.</title>
            <link>http://www.medworm.com/index.php?rid=4342836&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21199445%26dopt%3DAbstract</link>
            <description>This article highlights phenotypic features of schizophrenia that emerge from these studies and provides a neuropsychiatric perspective. Such efforts have helped elucidate potential neural substrates of deficits in cognition and affect in schizophrenia by providing measures of activation to neurobehavioral probes and connectivity among brain regions. Studies have demonstrated abnormalities at early stages of sensory processing that may influence downstream abnormalities in more complex evaluative functioning. The methodology can help bridge integration with neuropharmacologic, genomic, and neurorehabilitation investigations.
    PMID: 21199445 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342836</comments>
            <pubDate>Sun, 02 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342836</guid>        </item>
        <item>
            <title>Experimental Surgical Therapies for Huntington's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=4342838&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21199443%26dopt%3DAbstract</link>
            <description>Authors: Demeestere J, Vandenberghe W
    Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by abnormal movement, cognitive decline, and psychiatric disturbance. HD is caused by a trinucleotide repeat expansion in the HTT gene and a corresponding neurotoxic polyglutamine expansion in the huntingtin protein. There is currently no therapy to modify the progressive course of the disease, and symptomatic treatment options are limited. In this review we describe a diverse set of emerging experimental therapeutic strategies for HD: deep brain stimulation; delivery of neurotrophic factors; cell transplantation; HTT gene silencing using RNA interference or antisense oligonucleotides; and delivery of intrabodies. The common feature of these experimental the...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342838</comments>
            <pubDate>Tue, 28 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342838</guid>        </item>
        <item>
            <title>Parkinson's Disease Dementia and Potential Therapeutic Strategies.</title>
            <link>http://www.medworm.com/index.php?rid=4342837&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21199444%26dopt%3DAbstract</link>
            <description>Authors: Caviness JN, Lue L, Adler CH, Walker DG
    Dementia in Parkinson's disease (PD-D) has only been acknowledged in the recent three decades, but research in this field has accelerated. The purpose of this review was to discuss advances in PD-D regarding biomarker correlates and potential therapeutic targets. Attention and executive dysfunction, memory deficits that improve with cueing, and visual hallucinations are characteristic in PD-D. PD-D dramatically increases the disability and misery of the disease. Current treatment for PD-D is symptomatic, modest, and only transiently effective. There is wide agreement that more effective treatment is needed, but this will require more knowledge about PD-D pathophysiology. Advances in the pathogenesis of PD have focused on the substantia n...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342837</comments>
            <pubDate>Tue, 28 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342837</guid>        </item>
        <item>
            <title>Dysfunctional Brain Networks and Genetic Risk for Schizophrenia: Specific Neurotransmitter Systems.</title>
            <link>http://www.medworm.com/index.php?rid=4342834&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21199447%26dopt%3DAbstract</link>
            <description>Authors: Hirvonen J, Hietala J
    Multiple neurotransmitter circuits are disturbed in schizophrenia, and the dopamine hypothesis of schizophrenia prevails as the hypothesis with most empirical support. On the other hand, schizophrenia is highly heritable with a pattern consistent with both common and rare allelic variants and gene × environment interaction. Advances in the field of neuroimaging have expanded our knowledge of intermediate phenotypes, the neurobiological processes that convey the risk from the genes to the complex phenotype. In this article, we review the recent and continuously accumulating evidence from in vivo imaging studies aiming at characterizing neurochemical intermediate phenotypes of schizophrenia. Dopaminergic alterations in schizophrenia are shared by individua...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342834</comments>
            <pubDate>Tue, 28 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342834</guid>        </item>
        <item>
            <title>Description of Study Population and Analysis of Factors Influencing Adherence in the Observational Italian Study &quot;Evaluation of Pharmacotherapy Adherence in Bipolar Disorder&quot; (EPHAR).</title>
            <link>http://www.medworm.com/index.php?rid=4342833&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21199448%26dopt%3DAbstract</link>
            <description>Conclusions: The patient population of this observational trial was representative of the patients changing their therapy for bipolar disorder seen in clinical practice in Italy. Lack of adherence to pharmacotherapy for bipolar disorder is a serious issue, which is more likely to arise in alcohol users and patients with severe symptoms, negative attitude towards medication and/or initiation of treatment early in life. The findings could lead to a more adequate approach of adherence in patients with bipolar disorders.
    PMID: 21199448 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342833</comments>
            <pubDate>Tue, 28 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342833</guid>        </item>
        <item>
            <title>Dopamine Receptor Homooligomers and Heterooligomers in Schizophrenia.</title>
            <link>http://www.medworm.com/index.php?rid=4342832&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21199449%26dopt%3DAbstract</link>
            <description>Authors: Perreault ML, O'Dowd BF, George SR
    Over the past two decades the dopamine D2 receptor has been undoubtedly the most widely studied dopamine receptor for the therapeutic treatment of schizophrenia, as the majority of antipsychotics exhibit antagonism at this receptor. However, the cognitive symptoms of the disorder are mostly resistant to the majority of available antipsychotic treatments and, as a result, there is a critical need to develop novel therapies that ameliorate all symptoms. The recognition that dopamine receptors, such as all G protein-coupled receptors (GPCRs), exist as oligomeric complexes has provided new avenues for drug design in the search for novel therapies. Furthermore, that it is now known that dopamine receptors can form heteromers, such as the dopamine ...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342832</comments>
            <pubDate>Tue, 28 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342832</guid>        </item>
        <item>
            <title>The Upside of APP at Synapses.</title>
            <link>http://www.medworm.com/index.php?rid=4342835&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21199446%26dopt%3DAbstract</link>
            <description>Authors: Hoe HS, Lee HK, Pak DT
    The memory dysfunctions that characterize Alzheimer's disease (AD) are strongly correlated with synapse loss. The amyloid precursor protein (APP) and its cleavage product Aβ play central roles in synapse and memory loss, and thus are strongly implicated in the pathogenesis of AD. Numerous in vitro and transgenic AD mouse model studies have shown that overexpression of APP leads to Aβ accumulation, which causes decreased synaptic activity and dendritic spine density. However, the normal synaptic function of APP itself is not fully understood. Several recent studies have found that full-length APP promotes synaptic activity, synapse formation, and dendritic spine formation. These findings cast APP as a potential key player in learning and memory. It is o...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342835</comments>
            <pubDate>Mon, 27 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342835</guid>        </item>
        <item>
            <title>Revisiting the Diagnosis of Schizophrenia: Where have we been and Where are We Going?</title>
            <link>http://www.medworm.com/index.php?rid=4342831&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21199450%26dopt%3DAbstract</link>
            <description>This article focuses upon the classification of schizophrenia over the last 100 years, the current diagnosis of schizophrenia, changes for schizophrenia planned in the upcoming DSM 5, future directions for improving the diagnosis of schizophrenia, and the implications of a new diagnostic paradigm for the illness.
    PMID: 21199450 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342831</comments>
            <pubDate>Mon, 27 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342831</guid>        </item>
        <item>
            <title>Presynaptic Dopamine in Schizophrenia.</title>
            <link>http://www.medworm.com/index.php?rid=4342830&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21199451%26dopt%3DAbstract</link>
            <description>Authors: Miyake N, Thompson J, Skinbjerg M, Abi-Dargham A
    Presynaptic dopamine (DA) transmission has been measured in schizophrenia using different paradigms aimed at providing estimates of the integrity or the activity of the presynaptic dopaminergic neuron. Researchers have measured: (1) DA synthesis capacity with [(18) F]DOPA, a measure of the activity of dopa decarboxylase, (2) DA release with studies measuring the impact of a DA releasing stimulant challenge on the binding of a D(2) receptor radiotracer, (3) D(2) baseline occupancy by DA, a measure of baseline intrasynaptic DA, assessed by the changes in binding of D(2) radiotracer induced by DA depletion, and (4) the DA and the vesicular monoamine transporters, to assess the integrity of presynaptic terminals. The relationship be...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342830</comments>
            <pubDate>Mon, 27 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342830</guid>        </item>
        <item>
            <title>Clioquinol: Review of its Mechanisms of Action and Clinical Uses in Neurodegenerative Disorders.</title>
            <link>http://www.medworm.com/index.php?rid=4342829&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21199452%26dopt%3DAbstract</link>
            <description>Authors: Bareggi SR, Cornelli U
    Clioquinol was produced as a topical antiseptic and marketed as an oral intestinal amebicide in 1934, being used to treat a wide range of intestinal diseases. In the early 1970s, it was withdrawn from the market as an oral agent because of its association with subacute myelo-optic neuropathy (SMON), a syndrome that involves sensory and motor disturbances in the lower limbs and visual changes. The first methods for determining plasma and tissue clioquinol (5-chloro-7-iodo-8-quinolinol) levels were set up in the 1970s and involved HPLC separation with UV detection, these were followed by a more sensitive GC method with electron capture detection and a gaschromatographic-massspectrometric (GC-MS) method. Finally, an HPLC method using electrochemical detecti...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342829</comments>
            <pubDate>Mon, 27 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342829</guid>        </item>
        <item>
            <title>Tolerance to the Prophylactic Effects of Carbamazepine and Related Mood Stabilizers in the Treatment of Bipolar Disorders.</title>
            <link>http://www.medworm.com/index.php?rid=4342840&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21159150%26dopt%3DAbstract</link>
            <description>Authors: Post RM, Weiss SR
    Tolerance development after successful long-term treatment of bipolar disorder is under recognized, as are ways to prevent or show its occurrence or reverse it once it has occurred. We review the clinical literature which suggests that tolerance can develop to most treatment approaches in bipolar illness and present an animal model of tolerance development to anticonvulsant effects of carbamazepine or lamotrigine on amgydala-kindled seizures. In this model tolerance does not have a pharmacokinetic basis, but is contingent upon the drug being present in the brain at the time of amygdala stimulation. The occurrence of seizures in the absence of drug is sufficient to reverse tolerance and re-establish anticonvulsant efficacy. Based on the model, we hypothesize t...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342840</comments>
            <pubDate>Thu, 16 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342840</guid>        </item>
        <item>
            <title>Treatment of the Psychostimulant-Sensitized Animal Model of Schizophrenia.</title>
            <link>http://www.medworm.com/index.php?rid=4342839&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21159151%26dopt%3DAbstract</link>
            <description>Authors: Shuto T, Nishi A
    Behavioral sensitization to psychostimulants in rodents is associated with the alteration of dopaminergic neurotransmission, and has been proposed as a useful model of schizophrenia due to its progressively intensifying, easily relapsing, and long-lasting features. Pharmacological treatments that reverse the established sensitization may have potential therapeutic values for schizophrenia. The present aim is to review pharmacological treatments that induce the reversal of established sensitization to psychostimulants. In addition, we discuss possible mechanisms for the reversal of sensitization. Reversal of sensitization is induced by chronic dopamine D1 receptor agonism, D2 or D1/D2 receptor agonism combined with mild N-methyl-D-aspartate (NMDA) receptor anta...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342839</comments>
            <pubDate>Thu, 16 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342839</guid>        </item>
        <item>
            <title>The Noradrenergic Action in Antidepressant Treatments: Pharmacological and Clinical Aspects.</title>
            <link>http://www.medworm.com/index.php?rid=4342841&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21155988%26dopt%3DAbstract</link>
            <description>Authors: Dell'osso B, Palazzo MC, Oldani L, Altamura AC
    Even though noradrenaline has been recognized as one of the key neurotransmitters in the pathophysiology of major depression (MD), noradrenergic compounds have been less extensively utilized in clinical practice, compared to selective serotonin reuptake inhibitors (SSRIs). The development of the first selective noradrenergic reuptake inhibitor (NRI), Reboxetine, has not substantially changed the state of the art. In addition, Atomoxetine, a relatively pure NRI used for the treatment of ADHD, has shown mixed results when administered in augmentation to depressed subjects. Through a Medline search from 2000 to 2010, the present article provides an updated overview of the main pharmacological and clinical aspects of antidepressant cl...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342841</comments>
            <pubDate>Tue, 14 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342841</guid>        </item>
        <item>
            <title>HPA Axis Alterations in Mental Disorders: Impact on Memory and its Relevance for Therapeutic Interventions.</title>
            <link>http://www.medworm.com/index.php?rid=4342845&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21143429%26dopt%3DAbstract</link>
            <description>Authors: Wingenfeld K, Wolf OT
    Dysfunctions in hypothalamic-pituitary-adrenal (HPA) axis have been reported for several mental disorders that are also often characterized by memory disturbances. It is now well established that glucocorticoids influence cognitive processes by enhancing memory consolidation and impairing memory retrieval. There is further evidence for an association between HPA axis related disturbances and memory function in mental disorders. The present selective review provides a brief overview of HPA axis dysfunction and its impact on memory function in major depressive disorder, posttraumatic stress disorder, and borderline personality disorder. Furthermore, the relevance of these findings for therapeutic intervention is discussed.
    PMID: 21143429 [PubMed - as su...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342845</comments>
            <pubDate>Wed, 08 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342845</guid>        </item>
        <item>
            <title>Ginsenosides and Their CNS Targets.</title>
            <link>http://www.medworm.com/index.php?rid=4342844&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21143430%26dopt%3DAbstract</link>
            <description>Authors: Radad K, Moldzio R, Rausch WD
    Ginsenosides are a special group of triterpenoid saponins attributed to medical effects of ginseng. Therefore, they have been research targets over the last three decades to explain ginseng actions and a wealth of literature has been presented reporting on ginsenosides' effects on the human body. Recently, there is increasing evidence on beneficial effects of ginsenosides to the central nervous system (CNS). Using a wide range of in vitro and in vivo models, researchers have attributed these effects to specific pharmacological actions of ginsenosides on cerebral metabolism, oxidative stress and radical formation, neurotransmitter imbalance and membrane stabilizing effects, and even antiapoptotic effects. Modulating these particular mechanisms by g...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342844</comments>
            <pubDate>Wed, 08 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342844</guid>        </item>
        <item>
            <title>Antipsychotic Occupancy of Dopamine Receptors in Schizophrenia.</title>
            <link>http://www.medworm.com/index.php?rid=4342843&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21143431%26dopt%3DAbstract</link>
            <description>Authors: Nord M, Farde L
    Antipsychotic drugs were introduced in the early 50s on the basis of clinical observations in patients with schizophrenia. Experimental studies later revealed that antagonism at the D(2) dopamine receptor is a common characteristic of all antipsychotic drugs. In the 80s, the advent of brain imaging technologies such as positron emission tomography (PET) allowed for direct noninvasive studies of drug binding in treated patients. The concept receptor occupancy is defined as the fraction (%) of a receptor population that is occupied during treatment with an unlabelled drug. With regard to antipsychotic drugs, the radioligand [(11) C]-raclopride has been the most widely used for binding to the D(2) /D(3) -dopamine receptors. The present review discusses the contrib...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342843</comments>
            <pubDate>Wed, 08 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342843</guid>        </item>
        <item>
            <title>Brain Biochemical Effects of Methylphenidate Treatment Using Proton Magnetic Spectroscopy in Youth with Attention-Deficit Hyperactivity Disorder: A Controlled Pilot Study.</title>
            <link>http://www.medworm.com/index.php?rid=4342842&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21143432%26dopt%3DAbstract</link>
            <description>Conclusions: These preliminary findings suggest the presence of glutamatergic abnormalities in adolescents with ADHD, which may normalize with MPH treatment. Larger sample, controlled studies are needed to confirm these preliminary findings.
    PMID: 21143432 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342842</comments>
            <pubDate>Wed, 08 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4342842</guid>        </item>
        <item>
            <title>Therapeutic Potential of Kainate Receptors.</title>
            <link>http://www.medworm.com/index.php?rid=4251656&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21129167%26dopt%3DAbstract</link>
            <description>Authors: Matute C
    Glutamate receptors are key mediators of brain communication. Among ionotropic glutamate receptors, kainate receptors (KARs) have been least explored and their relevance to pathophysiology is relatively obscure. This is in part due to the relatively low abundance of KARs, the regulatory function in network activity they play, the lack of specific agonists and antagonists for this receptor subtype, as well as to the absence of striking phenotypes in mice deficient in KAR subunits. Nonetheless, it is now well established that KARs are located presynaptically whereby they regulate glutamate and GABA release, and thus, excitability and participate in short-term plasticity. In turn, KARs are also located postsynaptically and their activation contributes to synaptic integra...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4251656</comments>
            <pubDate>Mon, 06 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4251656</guid>        </item>
        <item>
            <title>Neuroprotection in Parkinson's disease: a realistic goal?</title>
            <link>http://www.medworm.com/index.php?rid=4154758&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21062424%26dopt%3DAbstract</link>
            <description>Authors: Galati S, Di Giovanni G
    
    PMID: 21062424 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4154758</comments>
            <pubDate>Thu, 11 Nov 2010 11:40:07 +0100</pubDate>
            <guid isPermaLink="false">4154758</guid>        </item>
        <item>
            <title>Histone Deacetylases and Mood Disorders: Epigenetic Programming in Gene-Environment Interactions.</title>
            <link>http://www.medworm.com/index.php?rid=4088717&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20961400%26dopt%3DAbstract</link>
            <description>Authors: Machado-Vieira R, Ibrahim L, Zarate CA
    Epigenetics involves molecular mechanisms related to gene expression independent of DNA sequence, mostly mediated by modification of chromatin histones. It has recently been suggested that these transcriptional changes may be implicated in the pathophysiology of mood disorders. In addition, histone deacetylase (HDAC) inhibitors have been shown to control epigenetic programming associated with the regulation of cognition and behavior, and may reverse dysfunctional epigenetic regulation associated with early life events in preclinical models. In this context, the active and continuous adaptation of chromatin, and the access of gene promoters to transcription factor mechanisms may represent a potential therapeutic target in the treatment of ...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4088717</comments>
            <pubDate>Tue, 19 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4088717</guid>        </item>
        <item>
            <title>Beneficial Effects of Electrostimulation Contingencies on Sustained Attention and Electrocortical Activity.</title>
            <link>http://www.medworm.com/index.php?rid=4088724&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20950324%26dopt%3DAbstract</link>
            <description>Conclusion: The results showed associations between acustimulation and improved perceptual sensitivity with sustained improvements following AE, but not LE stimulation. Improvements in commission errors in the AE group were related to the motor inhibition IC. The activational effects of acustimulation apparently attenuated the across-task habituation that characterized the control group.
    PMID: 20950324 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4088724</comments>
            <pubDate>Thu, 14 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4088724</guid>        </item>
        <item>
            <title>Electroacupuncture Protected Pyramidal Cells in Hippocampal CA1 Region of Vascular Dementia Rats by Inhibiting the Expression of P53 and Noxa.</title>
            <link>http://www.medworm.com/index.php?rid=4088723&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20950325%26dopt%3DAbstract</link>
            <description>Conclusions: The increasing expressions of p53 and Noxa play important roles in the pathogenesis of VD. EA improves learning and memory ability and protects pyramidal cells from apoptosis by blocking expression of p53 and Noxa in the hippocampal CA1 region of VD rats. These results suggest a novel mechanism of EA treatment to VD.
    PMID: 20950325 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4088723</comments>
            <pubDate>Thu, 14 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4088723</guid>        </item>
        <item>
            <title>Asenapine: A Review of Acute and Extension Phase Data in Bipolar Disorder.</title>
            <link>http://www.medworm.com/index.php?rid=4088722&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20950326%26dopt%3DAbstract</link>
            <description>Authors: McIntyre RS
    The second generation atypical antipsychotic, asenapine (Saphris), was approved by the US FDA (August 2009) for the acute treatment of manic or mixed episodes with or without psychotic features associated with bipolar I disorder in adults as well as the acute treatment of schizophrenia. Asenapine exhibits a high affinity for and antagonism at several serotonergic (5-HT(2A-C) , 5HT(5A) , 5HT(6) , 5HT(7) ), dopaminergic (D(2) , D(3) ), alpha-adrenergic (α(1) and α(2) ), and histaminergic (H1, H2) receptor subtypes. Asenapine is the first atypical antipsychotic formulated as a fast-dissolving, rapidly absorbed sublingual tablet. Asenapine was evaluated in adults with bipolar I disorder, manic or mixed episodes with or without psychotic features. Two identically desi...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4088722</comments>
            <pubDate>Thu, 14 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4088722</guid>        </item>
        <item>
            <title>Nanoparticulate Systems for Drug Delivery and Targeting to the Central Nervous System.</title>
            <link>http://www.medworm.com/index.php?rid=4088721&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20950327%26dopt%3DAbstract</link>
            <description>Authors: Craparo EF, Bondì ML, Pitarresi G, Cavallaro G
    Brain delivery is one of the major challenges for the neuropharmaceutical industry since an alarming increase in brain disease incidence is going on. Despite major advances in neuroscience, many potential therapeutic agents are denied access to the central nervous system (CNS) because of the existence of a physiological low permeable barrier, the blood-brain barrier (BBB). To obtain an improvement of drug CNS performance, sophisticated approaches such as nanoparticulate systems are rapidly developing. Many recent data demonstrate that drugs could be transported successfully into the brain using colloidal systems after i.v. injection by several mechanisms such as endocytosis or P-glycoprotein inhibition. This review summarizes the...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4088721</comments>
            <pubDate>Thu, 14 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4088721</guid>        </item>
        <item>
            <title>Role of Spinal Neurotransmitter Receptors in Itch: New Insights into Therapies and Drug Development.</title>
            <link>http://www.medworm.com/index.php?rid=4088720&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20950328%26dopt%3DAbstract</link>
            <description>Authors: Cevikbas F, Steinhoff M, Ikoma A
    Targets for antipruritic therapies are now expanding from the skin to the central nervous system. Recent studies demonstrate that various neuronal receptors in the spinal cord are involved in pruritus. The spinal opioid receptor is one of the best-known examples. Spinal administration of morphine is frequently accompanied by segmental pruritus. In addition to μ-opioid receptor antagonists, κ-opioid receptor agonists have recently come into usage as novel antipruritic drugs, and are expected to suppress certain subtypes of itch such as hemodialysis- and cholestasis-associated itch that are difficult to treat with antihistamines. The gastrin-releasing peptide receptor in the superficial dorsal horn of the spinal cord has also received recent at...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4088720</comments>
            <pubDate>Thu, 14 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4088720</guid>        </item>
        <item>
            <title>Efficacy of Rivastigmine on Executive Function in Patients with Parkinson's Disease Dementia.</title>
            <link>http://www.medworm.com/index.php?rid=4088719&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20950329%26dopt%3DAbstract</link>
            <description>Conclusion: Rivastigmine was associated with significant improvements over placebo on EF tests evaluating flexibility of thinking, problem solving and planning in patients with PDD. These findings support the hypothesis that rivastigmine may affect frontal subcortical circuits, which potentially contributes to observed clinical improvement associated with EF.
    PMID: 20950329 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4088719</comments>
            <pubDate>Thu, 14 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4088719</guid>        </item>
        <item>
            <title>Lacosamide and Epilepsy.</title>
            <link>http://www.medworm.com/index.php?rid=4088718&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20950330%26dopt%3DAbstract</link>
            <description>Authors: Harris JA, Murphy JA
    We will review all available studies on the use of lacosamide in the treatment of partial-onset seizures. The available evidence includes two open-label studies and three randomized controlled trials evaluating the safety and efficacy of oral lacosamide. One open-label study and one randomized controlled trial evaluating the safety and tolerability of intravenous lacosamide was also identified. Lacosamide was found to be efficacious with significant reduction in seizure frequency dosed 400-600 mg daily. Moreover, its adverse drug effects were mild and infrequently reported in the literature. Findings suggest that lacosamide is an effective agent for adjunctive treatment of refractory partial-onset seizures.
    PMID: 20950330 [PubMed - as supplied by publi...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4088718</comments>
            <pubDate>Thu, 14 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4088718</guid>        </item>
        <item>
            <title>Sevoflurane Postconditioning Ameliorates Oxygen-Glucose Deprivation-Reperfusion Injury in the Rat Hippocampus.</title>
            <link>http://www.medworm.com/index.php?rid=4027256&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20875045%26dopt%3DAbstract</link>
            <description>Conclusion: Postconditioning with sevoflurane reduces neuronal damage after OGD-reperfusion injury in the CA1 area of rat hippocampus, in vitro.
    PMID: 20875045 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4027256</comments>
            <pubDate>Mon, 27 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4027256</guid>        </item>
        <item>
            <title>Peculiarities of Geriatric Psychiatry: A Focus on Aging and Depression.</title>
            <link>http://www.medworm.com/index.php?rid=4027255&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20875046%26dopt%3DAbstract</link>
            <description>Authors: Laks J, Engelhardt E
    There is a debate on whether Geriatric Psychiatry stands for itself as a discrete specialty or whether it is an extension of clinical Geriatrics, Neurology, and Psychiatry. This review aims to outline some recent data and possible approaches to define peculiarities of Geriatric Psychiatry, focusing on certain characteristics that define the aging brain. Geriatric depression is discussed taking into consideration some data from translational research. The brain aging process is not uniform. Frontal areas show marked impairment in inhibiting irrelevant information in working memory as they age, and the recruitment of these areas occur differently than in young subjects. Executive functions also change in normal elderly. Geriatric depression is a general defi...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4027255</comments>
            <pubDate>Mon, 27 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4027255</guid>        </item>
        <item>
            <title>The Multiplicity of Action of Cannabinoids: Implications for Treating Neurodegeneration.</title>
            <link>http://www.medworm.com/index.php?rid=4027254&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20875047%26dopt%3DAbstract</link>
            <description>This article will discuss the experimental and clinical evidence supporting a potential role for CB-based therapies in the treatment of certain neurological diseases that feature a neurodegenerative component.
    PMID: 20875047 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4027254</comments>
            <pubDate>Mon, 27 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4027254</guid>        </item>
        <item>
            <title>Genomics and Pharmacogenomics of Dementia.</title>
            <link>http://www.medworm.com/index.php?rid=3885653&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20718828%26dopt%3DAbstract</link>
            <description>Authors: Cacabelos R, MartÃ­nez-Bouza R
    SUMMARY Dementia is a major problem of health in developed countries, and a prototypical paradigm of chronic disability, high cost, and social-family burden. Approximately, 10-20% of direct costs in this kind of neuropathology are related to pharmacological treatment, with a moderate responder rate below 30% and questionable cost-effectiveness. Over 200 different genes have been associated with the pathogenesis of dementia. Studies on structural and functional genomics, transcriptomics, proteomics and metabolomics have revealed the paramount importance of these novel technologies for the understanding of pathogenic cascades and the prediction of therapeutic outcomes in dementia. About 10-30% of Western populations are defective in genes of the ...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3885653</comments>
            <pubDate>Sun, 15 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3885653</guid>        </item>
        <item>
            <title>Genomics and Pharmacogenomics of Schizophrenia.</title>
            <link>http://www.medworm.com/index.php?rid=3885652&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20718829%26dopt%3DAbstract</link>
            <description>Authors: Cacabelos R, MartÃ­nez-Bouza R
    SUMMARY Schizophrenia (SCZ) is among the most disabling of mental disorders. Several neurobiological hypotheses have been postulated as responsible for SCZ pathogenesis: polygenic/multifactorial genomic defects, intrauterine and perinatal environment-genome interactions, neurodevelopmental defects, dopaminergic, cholinergic, serotonergic, gamma-aminobutiric acid (GABAergic), neuropeptidergic and glutamatergic/N-Methyl-D-Aspartate (NMDA) dysfunctions, seasonal infection, neuroimmune dysfunction, and epigenetic dysregulation. SCZ has a heritability estimated at 60-90%. Genetic studies in SCZ have revealed the presence of chromosome anomalies, copy number variants, multiple single-nucleotide polymorphisms of susceptibility distributed across the h...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3885652</comments>
            <pubDate>Sun, 15 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3885652</guid>        </item>
        <item>
            <title>A Double-Blind, Randomized, Placebo and Active-Controlled Study of Nebicapone for the Treatment of Motor Fluctuations in Parkinson's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3795521&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20653695%26dopt%3DAbstract</link>
            <description>Authors: Ferreira JJ, Rascol O, Poewe W, Sampaio C, Rocha JF, Nunes T, Almeida L, Soares-da-Silva P, 
    To determine the efficacy, safety and tolerability of nebicapone, a new catechol-O-methyltransferase inhibitor for the treatment of motor fluctuations in Parkinson's disease (PD), we conducted a multicenter, randomized, 8-week double-blind, placebo- and active-controlled, parallel-group study comparing nebicapone 50 mg, 100 mg, or 150 mg, entacapone 200 mg (active control) or placebo administered concomitantly with levodopa/carbidopa or levodopa/benserazide. Two hundred and fifty-two PD patients with motor fluctuations treated with levodopa/carbidopa or levodopa/benserazide (4-8 daily doses) were enrolled and 250 patients were eligible for intention-to-treat (ITT) analysis on the basis...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3795521</comments>
            <pubDate>Thu, 22 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3795521</guid>        </item>
        <item>
            <title>Targeting Histone Deacetylases for the Treatment of Huntington's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3777613&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20642797%26dopt%3DAbstract</link>
            <description>Authors: Gray SG
    SUMMARY Huntington's disease is a debilitating neurodegenerative condition with significant burdens on both patient and healthcare costs. Despite the identification of the causative element, an expanded toxic polyglutamine tract in the mutant Huntingtin protein, treatment options for patients with this disease remain limited. In the following review I assess the current evidence suggesting that a family of important regulatory proteins known as histone deacetylases may be an important therapeutic target in the treatment of this disease.
    PMID: 20642797 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3777613</comments>
            <pubDate>Tue, 13 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3777613</guid>        </item>
        <item>
            <title>Neurosyphilis: A Historical Perspective and Review.</title>
            <link>http://www.medworm.com/index.php?rid=3761780&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20626434%26dopt%3DAbstract</link>
            <description>Authors: Ghanem KG
    SUMMARY Treponema pallidum subspecies pallidum, the causative agent of syphilis, disseminates to the central nervous system within days after exposure. Clinical manifestations can occur during any stage of the infection, and include asymptomatic neurosyphilis, acute meningeal syphilis, meningovascular syphilis, paretic neurosyphilis, and tabetic neurosyphilis. The majority of cases are reported in HIV-infected patients but the epidemiology of modern neurosyphilis is not well defined because of the paucity of population-based data. Decreasing reports of late neurosyphilis have been countered with increasing reports of early neurologic involvement. This review summarizes the clinical manifestations, diagnosis, and therapy of neurosyphilis, focusing on areas of continue...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761780</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761780</guid>        </item>
        <item>
            <title>Downregulation and Upregulation of Glial Connexins May Cause Synaptic Imbalances Responsible for the Pathophysiology of Bipolar Disorder.</title>
            <link>http://www.medworm.com/index.php?rid=3761779&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20626435%26dopt%3DAbstract</link>
            <description>Authors: Mitterauer BJ
    SUMMARY The model of the pathophysiology of bipolar disorder proposed is based on imbalances in tripartite synapses caused by dysregulations of connexin expression in the astrocytic syncytium. If the expression of connexins is downregulated, a compensatory upregulation of astrocytic receptors may occur and be responsible for the pathophysiology of depression. Conversely, if the expression of connexins is upregulated, the expression of the astrocytic receptors may be downregulated and be responsible for the pathophysiology of mania. In depression, a relative lack of neurotransmitters exerts a protracted synaptic information processing, whereas in mania a relative increase of neurotransmitters may accelerate synaptic information processing. In addition, the modulat...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761779</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761779</guid>        </item>
        <item>
            <title>Brain Stimulation: New Vistas for the Exploration and Treatment of Tinnitus.</title>
            <link>http://www.medworm.com/index.php?rid=3761778&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20626436%26dopt%3DAbstract</link>
            <description>Conclusions: These proof of principle studies point toward a new option for the investigation and neurophysiology based treatment of tinnitus. Based on these findings, larger scale randomized clinical trials are needed to explore the efficacy of different brain stimulation techniques and parameters as well as the optimal target sites and treatment schedules. Particularly, a careful evaluation of clinical relevance under consideration of an adequate sham control and attention to possible unwanted side effects of these new interventions are indispensable.
    PMID: 20626436 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761778</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761778</guid>        </item>
        <item>
            <title>Oxytocin: Crossing the Bridge between Basic Science and Pharmacotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=3761788&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20626426%26dopt%3DAbstract</link>
            <description>Authors: Viero C, Shibuya I, Kitamura N, Verkhratsky A, Fujihara H, Katoh A, Ueta Y, Zingg HH, Chvatal A, Sykova E, Dayanithi G
    SUMMARY Is oxytocin the hormone of happiness? Probably not. However, this small nine amino acid peptide is involved in a wide variety of physiological and pathological functions such as sexual activity, penile erection, ejaculation, pregnancy, uterus contraction, milk ejection, maternal behavior, osteoporosis, diabetes, cancer, social bonding, and stress, which makes oxytocin and its receptor potential candidates as targets for drug therapy. In this review, we address the issues of drug design and specificity and focus our discussion on recent findings on oxytocin and its heterotrimeric G protein-coupled receptor OTR. In this regard, we will highlight the foll...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761788</comments>
            <pubDate>Tue, 06 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761788</guid>        </item>
        <item>
            <title>The Genetics of White Matter Lesions.</title>
            <link>http://www.medworm.com/index.php?rid=3761787&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20626427%26dopt%3DAbstract</link>
            <description>Authors: Assareh A, Mather KA, Schofield PR, Kwok JB, Sachdev PS
    White matter lesions (WMLs), commonly seen as hyperintensities on T2-weighted MRI scans of healthy elderly individuals, are considered to be related to small vessel disease in the brain, and are often associated with subtle cognitive and functional impairments. WMLs also show a strong correlation with a wide range of neurodegenerative and neuropsychiatric disorders. Although a number of vascular risk factors for WMLs have been identified, genetic factors are also important with twin and family studies reporting high heritability. Mutations in several genes have been described that lead to monogenic disorders manifesting WMLs, such as Fabry disease and CADASIL. Because most individuals with WMLs do not have Mendelian disor...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761787</comments>
            <pubDate>Tue, 06 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761787</guid>        </item>
        <item>
            <title>The Combination of Interferon-Beta and HMG-CoA Reductase Inhibition in Multiple Sclerosis: Enthusiasm Lost too Soon?</title>
            <link>http://www.medworm.com/index.php?rid=3761786&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20626428%26dopt%3DAbstract</link>
            <description>Authors: Sellner J, Weber MS, Vollmar P, Mattle HP, Hemmer B, StÃ¼ve O
    SUMMARY Recent studies support the notion that statins, widely prescribed cholesterol-lowering agents, may target key elements in the immunological cascade leading to inflammation and tissue damage in the pathogenesis of multiple sclerosis (MS). Compelling experimental and observational clinical studies highlighted the possibility that statins may also exert immunomodulatory synergy with approved MS drugs, resulting in several randomized clinical trials testing statins in combination with interferon-beta (IFN-beta). Some data, however, suggest that this particular combination may not be clinically beneficial, and might actually have a negative effect on the disease course in some patients with MS. In this regard, ...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761786</comments>
            <pubDate>Tue, 06 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761786</guid>        </item>
        <item>
            <title>Neuropsychiatric Adverse Effects of Centrally Acting Antiobesity Drugs.</title>
            <link>http://www.medworm.com/index.php?rid=3761785&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20626429%26dopt%3DAbstract</link>
            <description>Conclusion: These findings highlight the need to assess neuropsychiatric adverse events comprehensively using sensitive and validated methods early in the clinical development of candidate antiobesity drugs with a central mechanism of action.
    PMID: 20626429 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761785</comments>
            <pubDate>Tue, 06 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761785</guid>        </item>
        <item>
            <title>The Use of Antidepressants for Headache Prophylaxis.</title>
            <link>http://www.medworm.com/index.php?rid=3761784&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20626430%26dopt%3DAbstract</link>
            <description>Authors: Smitherman TA, Walters AB, Maizels M, Penzien DB
    SUMMARY The focus of this review is on the efficacy of antidepressants as preventive treatments for migraine and chronic tension-type headache (TTH). Pharmacologic prophylaxis may be indicated for patients with frequent headaches, who respond insufficiently to acute therapies, or for whom medication overuse is a concern. The well-documented efficacy of the tricyclic antidepressant amitriptyline, both for migraine and chronic TTH, has been followed by widespread use of other antidepressants for headache prophylaxis. Although antidepressants in general share comparable efficacy for the treatment of depressive disorders, their efficacy as headache preventives varies widely. Evidence supporting use of the selective serotonin reuptak...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761784</comments>
            <pubDate>Tue, 06 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761784</guid>        </item>
        <item>
            <title>Hypothermia Reduces Brain Edema, Spontaneous Recurrent Seizure Attack, and Learning Memory Deficits in the Kainic Acid Treated Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3761783&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20626431%26dopt%3DAbstract</link>
            <description>Conclusions: Hypothermia treatment immediately after SE not only exhibited protective effects against the chronic spontaneous recurrent convulsant seizures but also improved cognitive function. These antiepileptogenic properties of hypothermia may be related to its attenuating effect on brain edema induced by SE. They therefore suggest that brain edema may be involved in the progress of epileptogenesis.
    PMID: 20626431 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761783</comments>
            <pubDate>Tue, 06 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761783</guid>        </item>
        <item>
            <title>Acute Drug Administration in Epilepsy: A Review.</title>
            <link>http://www.medworm.com/index.php?rid=3761782&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20626432%26dopt%3DAbstract</link>
            <description>Conclusions: The best evidence for the efficacy of ADA exists in febrile and nonfebrile childhood seizures, whereas the evidence in catamenial epilepsy is weak. Prevention of clusters is a well-proven principle but its application has been little studied. Prevention of imminent seizures predicted by well-established triggers, defined risk factors, or premonitory minor seizure activity seems to be at the same time the most intelligent and the least investigated application of ADA and would deserve to be better studied.
    PMID: 20626432 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761782</comments>
            <pubDate>Tue, 06 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761782</guid>        </item>
        <item>
            <title>Effects of Cholinesterase Inhibitors in Parkinson's Disease Dementia: A Review of Clinical Data.</title>
            <link>http://www.medworm.com/index.php?rid=3761781&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20626433%26dopt%3DAbstract</link>
            <description>Conclusions: Taken together, these studies suggest that ChEIs are efficacious in the treatment of PDD.
    PMID: 20626433 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761781</comments>
            <pubDate>Tue, 06 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761781</guid>        </item>
        <item>
            <title>Beyond the Cholinergic Hypothesis: Do Current Drugs Work in Alzheimer's Disease?</title>
            <link>http://www.medworm.com/index.php?rid=3691987&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20560995%26dopt%3DAbstract</link>
            <description>Authors: Martorana A, Esposito Z, Koch G
    SUMMARY Alzheimer's disease (AD) is a neurodegenerative disease characterized by memory and cognitive loss, and represents the leading cause of dementia in elderly people. Besides the complex biochemical processes involved in the neuronal degeneration (formation of senile plaques containing Abeta peptides, and development of neurofibrillary tangles), other molecular and neurochemical alterations, like cholinergic deficit due to basal forebrain degeneration, also occur. Because acetylcholine has been demonstrated to be involved in cognitive processes, the idea to increase acetylcholine levels to restore cognitive deficits has gained interest (the so-called cholinergic hypothesis). This has led to the development of drugs able to prevent acetylcho...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3691987</comments>
            <pubDate>Thu, 17 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3691987</guid>        </item>
        <item>
            <title>All Roads to Schizophrenia Lead to Dopamine Supersensitivity and Elevated Dopamine D2 Receptors.</title>
            <link>http://www.medworm.com/index.php?rid=3691986&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20560996%26dopt%3DAbstract</link>
            <description>Conclusions: These multiple abnormal pathways converge to a final common pathway of dopamine supersensitivity and elevated D2(High) receptors, presumably responsible for psychotic symptoms. Although antipsychotics alleviate psychosis and reverse the elevation of D2(High) receptors, long-term antipsychotics can further enhance dopamine supersensitivity in patients. Therefore, switching from a traditional antipsychotic to an agonist antipsychotic (aripiprazole) can result in psychotic signs and symptoms. Clozapine and quetiapine do not elicit parkinsonism or tardive dyskinesia because they are released from D2 within 12 to 24 h. Traditional antipsychotics remain attached to D2 receptors for days, preventing relapse, but allowing accumulation that can lead to tardive dyskinesia. Future goals ...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3691986</comments>
            <pubDate>Thu, 17 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3691986</guid>        </item>
        <item>
            <title>Zopiclone (Cyclopyrrolone): A Novel Hypnosedative; Hypnosedation Caused by Zopiclone Does Not Impair Memory-Learning in Albino Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3691990&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20560992%26dopt%3DAbstract</link>
            <description>Conclusions: Zopiclone (7.5 mg/kg p.o.) has selective hypnosedative activity but not CNS-depressant activity similar to BZDs. Hypnosedative action of Zopiclone does not impair memory-learning in albino mice like conventional hypnosedatives.
    PMID: 20560992 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3691990</comments>
            <pubDate>Tue, 15 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3691990</guid>        </item>
        <item>
            <title>gamma-Secretase Inhibitors for the Treatment of Alzheimer's Disease: The Current State.</title>
            <link>http://www.medworm.com/index.php?rid=3691989&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20560993%26dopt%3DAbstract</link>
            <description>Conclusions: Unfortunately, gamma-secretase inhibitors may cause intestinal goblet cell hyperplasia, thymus atrophy, decrease in lymphocytes, and alterations in hair color, effects associated with the inhibition of the cleavage of Notch, a protein involved in cell development and differentiation. Nevertheless, at least other two promising gamma-secretase inhibitors are being tested clinically. This class of drugs represents a major hope to slow the rate of decline of AD.
    PMID: 20560993 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3691989</comments>
            <pubDate>Tue, 15 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3691989</guid>        </item>
        <item>
            <title>The Role of Dopamine in Symptoms and Treatment of Apathy in Alzheimer's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3691988&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20560994%26dopt%3DAbstract</link>
            <description>Authors: Mitchell RA, Herrmann N, LanctÃ´t KL
    SUMMARY Background: Alzheimer's disease (AD) is characterized by a number of serious and debilitating behavioral and psychological symptoms of dementia (BPSD). The most common of these BPSD is apathy, which represents a major source of morbidity and premature institutionalization in the AD population. Many studies have identified discrete changes to the dopaminergic (DAergic) system in patients with AD. The DAergic system is closely related to the brain reward system (BRS) and some studies have suggested that dysfunction in the DAergic system may account for symptoms of apathy in the AD population. Method: Changes to the dopamine (DA) system in AD will be reviewed, and evidence supporting the involvement of the DAergic system in the devel...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3691988</comments>
            <pubDate>Tue, 15 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3691988</guid>        </item>
        <item>
            <title>Apoptosis-Inducing Factor and Cyclophilin A Cotranslocate to the Motor Neuronal Nuclei in Amyotrophic Lateral Sclerosis Model Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3677034&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20553309%26dopt%3DAbstract</link>
            <description>Conclusions: From these results, we suggest that CypA and AIF may play cooperative and pivotal roles in motor neuronal death in the murine ALS model.
    PMID: 20553309 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677034</comments>
            <pubDate>Sun, 13 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677034</guid>        </item>
        <item>
            <title>The Role of Tau in Alzheimer's Disease and Related Disorders.</title>
            <link>http://www.medworm.com/index.php?rid=3677033&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20553310%26dopt%3DAbstract</link>
            <description>Authors: Medeiros R, Baglietto-Vargas D, Laferla FM
    SUMMARY Tau, the microtubule-associated protein, forms insoluble filaments that accumulate as neurofibrillary tangles in Alzheimer's disease (AD) and related tauopathies. Under physiological conditions, tau regulates the assembly and maintenance of the structural stability of microtubules. In the diseased brain, however, tau becomes abnormally hyperphosphorylated, which ultimately causes the microtubules to disassemble, and the free tau molecules aggregate into paired helical filaments. A large body of evidence suggests that tau hyperphosphorylation results from perturbation of cellular signaling, mainly through imbalance in the activities of different protein kinases and phosphatases. In AD, it appears that ss-amyloid peptide (Ass) p...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677033</comments>
            <pubDate>Sun, 13 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677033</guid>        </item>
        <item>
            <title>Effects of Exogenous Agents on Brain Development: Stress, Abuse and Therapeutic Compounds.</title>
            <link>http://www.medworm.com/index.php?rid=3677032&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20553311%26dopt%3DAbstract</link>
            <description>Authors: Archer T
    SUMMARY The range of exogenous agents likely to affect, generally detrimentally, the normal development of the brain and central nervous system defies estimation although the amount of accumulated evidence is enormous. The present review is limited to certain types of chemotherapeutic and &quot;use-and-abuse&quot; compounds and environmental agents, exemplified by anesthetic, antiepileptic, sleep-inducing and anxiolytic compounds, nicotine and alcohol, and stress as well as agents of infection; each of these agents have been investigated quite extensively and have been shown to contribute to the etiopathogenesis of serious neuropsychiatric disorders. To greater or lesser extent, all of the exogenous agents discussed in the present treatise have been investigated for their influ...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677032</comments>
            <pubDate>Sun, 13 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677032</guid>        </item>
        <item>
            <title>Mapping Brain Metals to Evaluate Therapies for Neurodegenerative Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3677031&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20553312%26dopt%3DAbstract</link>
            <description>Authors: Gh Popescu BF, Nichol H
    The brain is rich in metals and has a high metabolic rate, making it acutely vulnerable to the toxic effects of endogenously produced free radicals. The abundant metals, iron and copper, transfer single electrons as they cycle between their reduced (Fe(2+), Cu(1+)) and oxidized (Fe(3+), Cu(2+)) states making them powerful catalysts of reactive oxygen species (ROS) production. Even redox inert zinc, if present in excess, can trigger ROS production indirectly by altering mitochondrial function. While metal chelators seem to improve the clinical outcome of several neurodegenerative diseases, their mechanisms of action remain obscure and the effects of long-term use are largely unknown. Most chelators are not specific to a single metal and could alter the d...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677031</comments>
            <pubDate>Sun, 13 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677031</guid>        </item>
        <item>
            <title>An Approach for Neuroprotective Therapies of Secondary Brain Damage after Excitotoxic Retinal Injury in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3677041&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20553302%26dopt%3DAbstract</link>
            <description>Conclusion: In this review, we describe time-dependent alterations in the visual center in brain following RGCs loss, and whether some drugs prevent the neuronal damage of the visual center in the brain.
    PMID: 20553302 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677041</comments>
            <pubDate>Thu, 10 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677041</guid>        </item>
        <item>
            <title>The Role of Inflammation in the Pathogenesis of Delirium and Dementia in Older Adults: A Review.</title>
            <link>http://www.medworm.com/index.php?rid=3677040&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20553303%26dopt%3DAbstract</link>
            <description>Conclusion: Mounting evidence supports the role of inflammation in the development of both dementia and delirium. Further studies are needed to elucidate the mechanisms underlying these relationships.
    PMID: 20553303 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677040</comments>
            <pubDate>Thu, 10 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677040</guid>        </item>
        <item>
            <title>Antidepressant-Induced Suicidality: An Update.</title>
            <link>http://www.medworm.com/index.php?rid=3677039&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20553304%26dopt%3DAbstract</link>
            <description>This article provides an update of the controversy surrounding antidepressants as a potential cause of suicidal ideations or behavior. Antidepressant-induced suicidality appears to be an uncommon occurrence but also a legitimate phenomenon. Close monitoring and a follow-up care should be provided for patients after initiation of a new antidepressant.
    PMID: 20553304 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677039</comments>
            <pubDate>Thu, 10 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677039</guid>        </item>
        <item>
            <title>Role of Zolpidem in the Management of Insomnia.</title>
            <link>http://www.medworm.com/index.php?rid=3677038&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20553305%26dopt%3DAbstract</link>
            <description>Authors: Dang A, Garg A, Rataboli PV
    Insomnia is a common condition that affects one's ability to sleep comfortably and consequently to work effectively. Its etiology is multifactorial and involves plethora of risk factors. Consequences can vary from mild sleepiness to more sever psychiatric disturbances and ischemic stroke. Despite several diagnostic criteria it is poorly diagnosed and less often treated. Benzodiazepines formed the mainline therapy for many years till the advent of newer nonbenzodiazepine group of drugs including zolpidem. Zolpidem is an imidazo-pyridine compound that enhances the GABA(A) receptor function by interaction with Omega-1 receptor subtype. Its pharmacokinetic profile allows the patients to use it later in the night when having trouble falling asleep withou...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677038</comments>
            <pubDate>Thu, 10 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677038</guid>        </item>
        <item>
            <title>Seeking Brain Biomarkers for Preventive Therapy in Huntington Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3677037&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20553306%26dopt%3DAbstract</link>
            <description>Authors: Esmaeilzadeh M, Ciarmiello A, Squitieri F
    Huntington disease (HD) is a severe incurable nervous system disease that generally has an onset age of around 35-50, and is caused by a dominantly transmitted expansion mutation. A genetic test allows persons at risk, i.e., offspring or siblings of affected individuals, to discover their genetic status. Unaffected mutation-positive subjects will manifest HD sometime during life. Despite major advances in research on pathogenic mechanisms, no studies have yet fully validated preventive therapy or biomarkers for use before the symptoms become clinically manifest. Seeking brain and peripheral biomarkers is a requisite to develop a cure for HD. Changes in the brain can be observed in vivo using methods such as structural magnetic resonanc...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677037</comments>
            <pubDate>Thu, 10 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677037</guid>        </item>
        <item>
            <title>Dimebolin in Dementia.</title>
            <link>http://www.medworm.com/index.php?rid=3677036&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20553307%26dopt%3DAbstract</link>
            <description>This article considers various theories proposed to explain its effect in the treatment of dementia. The results from further trials will help to clarify the future of dimebolin as a potential treatment for chronic neurodegenerative disorders that include dementia that affects 25 million people worldwide.
    PMID: 20553307 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677036</comments>
            <pubDate>Thu, 10 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677036</guid>        </item>
        <item>
            <title>Genome-Wide Findings in Schizophrenia and the Role of Gene-Environment Interplay.</title>
            <link>http://www.medworm.com/index.php?rid=3677035&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20553308%26dopt%3DAbstract</link>
            <description>Authors: van Winkel R, Esquivel G, Kenis G, Wichers M, Collip D, Peerbooms O, Rutten B, Myin-Germeys I, van Os J
    The recent advent of genome-wide mass-marker technology has resulted in renewed optimism to unravel the genetic architecture of psychotic disorders. Genome-wide association studies have identified a number of common polymorphisms robustly associated with schizophrenia, in ZNF804A, transcription factor 4, major histocompatibility complex, and neurogranin. In addition, copy number variants (CNVs) in 1q21.1, 2p16.3, 15q11.2, 15q13.3, 16p11.2, and 22q11.2 were convincingly implicated in schizophrenia risk. Furthermore, these studies have suggested considerable genetic overlap with bipolar disorder (particularly for common polymorphisms) and neurodevelopmental disorders such as a...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677035</comments>
            <pubDate>Thu, 10 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677035</guid>        </item>
        <item>
            <title>Steroids-dopamine interactions in the pathophysiology and treatment of CNS disorders.</title>
            <link>http://www.medworm.com/index.php?rid=3677030&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20557567%26dopt%3DAbstract</link>
            <description>Conclusion: Clinical and experimental evidence supports a role of steroid-dopamine interactions in the pathophysiology of schizophrenia, depression and Parkinson's disease. Specific steroidal receptor agonists and SERMs are available for endocrine and cancer treatments and could find other applications as adjunct treatments in central nervous system diseases.
    PMID: 20557567 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677030</comments>
            <pubDate>Mon, 31 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677030</guid>        </item>
        <item>
            <title>Dopamine and oxytocin interactions underlying behaviors: potential contributions to behavioral disorders.</title>
            <link>http://www.medworm.com/index.php?rid=3677029&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20557568%26dopt%3DAbstract</link>
            <description>Authors: Baskerville TA, Douglas AJ
    Dopamine is an important neuromodulator that exerts widespread effects on the central nervous system (CNS) function. Disruption in dopaminergic neurotransmission can have profound effects on mood and behavior and as such is known to be implicated in various neuropsychiatric behavioral disorders including autism and depression. The subsequent effects on other neurocircuitries due to dysregulated dopamine function have yet to be fully explored. Due to the marked social deficits observed in psychiatric patients, the neuropeptide, oxytocin is emerging as one particular neural substrate that may be influenced by the altered dopamine levels subserving neuropathologic-related behavioral diseases. Oxytocin has a substantial role in social attachment, affilia...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677029</comments>
            <pubDate>Mon, 31 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677029</guid>        </item>
        <item>
            <title>Dopamine Interaction with other Neurotransmitter Systems: Relevance in the Pathophysiology and Treatment of CNS Disorders.</title>
            <link>http://www.medworm.com/index.php?rid=3677028&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20557569%26dopt%3DAbstract</link>
            <description>Authors: Di Giovanni G
    
    PMID: 20557569 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677028</comments>
            <pubDate>Mon, 31 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677028</guid>        </item>
        <item>
            <title>Role of serotonin in central dopamine dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=3677027&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20557570%26dopt%3DAbstract</link>
            <description>Authors: Di Giovanni G, Esposito E, Di Matteo V
    The interaction between serotonin (5-HT) and dopamine (DA)-containing neurons in the brain is a research topic that has raised the interest of many scientists working in the field of neuroscience since the first demonstration of the presence of monoamine-containing neurons in the mid 1960. The bulk of neuroanatomical data available clearly indicate that DA-containing neurons in the brain receive a prominent innervation from serotonin (5-hydroxytryptamine, 5-HT) originating in the raphe nuclei of the brainstem. Compelling electrophysiological and neurochemical data show that 5-HT can exert complex effects on the activity of midbrain DA neurons mediated by its various receptor subtypes. The main control seems to be inhibitory, this effect b...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677027</comments>
            <pubDate>Mon, 31 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677027</guid>        </item>
        <item>
            <title>UFP-112 a Potent and Long-Lasting Agonist Selective for the Nociceptin/Orphanin FQ Receptor.</title>
            <link>http://www.medworm.com/index.php?rid=3600189&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20497197%26dopt%3DAbstract</link>
            <description>Authors: Calo' G, Rizzi A, Cifani C, Di Bonaventura MV, Regoli D, Massi M, Salvadori S, Lambert DG, Guerrini R
    Nociceptin/orphanin FQ (N/OFQ) controls several biological functions via selective activation of the N/OFQ peptide receptor (NOP). [(pF)Phe(4)Aib(7)Arg(14)Lys(15)]N/OFQ-NH(2) (UFP-112) is an NOP receptor ligand designed using a combination of several chemical modifications in the same peptide sequence that increase NOP receptor affinity/potency and/or reduce susceptibility to enzymatic degradation. In the present review article, we summarize data from the literature and present original findings on the in vitro and in vivo pharmacological features of UFP-112. Moreover, important biological actions and possible therapeutic indications of NOP receptor agonists are discussed base...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3600189</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3600189</guid>        </item>
        <item>
            <title>Pharmacological Therapy in Parkinson's Disease: Focus on Neuroprotection.</title>
            <link>http://www.medworm.com/index.php?rid=3531470&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20438581%26dopt%3DAbstract</link>
            <description>Authors: Kincses ZT, Vecsei L
    Although the number of available therapeutic approaches in Parkinson's disease (PD) is steadily increasing the search for effective neuroprotective agent is continuing. Such research is directed at influencing the key steps in the pathomechanism: the mitochondrial dysfunction, the oxidative stress, the neuroinflammatory processes and the final common apoptotic pathway. Earlier-developed symptomatic therapies were implicated to be neuroprotective, and promising novel disease modifying approaches were brought into the focus of interest. The current review presents a survey of our current knowledge relating to the pathomechanism of PD and discusses the putative neuroprotective therapy.
    PMID: 20438581 [PubMed - as supplied by publisher] (Source: CNS Neuros...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3531470</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3531470</guid>        </item>
        <item>
            <title>GABA-A Receptor Modulators: Can they Offer any Improvement over Benzodiazepines in the Treatment of Anxiety Disorders?</title>
            <link>http://www.medworm.com/index.php?rid=3508619&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20415836%26dopt%3DAbstract</link>
            <description>Authors: Iosifescu DV
    
    PMID: 20415836 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508619</comments>
            <pubDate>Wed, 31 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508619</guid>        </item>
        <item>
            <title>The prevalence of migraine headaches in an anxiety disorders clinic sample.</title>
            <link>http://www.medworm.com/index.php?rid=3508618&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20415837%26dopt%3DAbstract</link>
            <description>This study suggests that there is an increased prevalence of migraine headaches among anxiety disorder patients as compared to the general population. Migraine comorbidity may have important clinical implications, such that the treatment of one condition could potentially ameliorate the development or progression of the other. Further research is required to better understand the nature and implications of the association between migraine and psychiatric disorders.
    PMID: 20415837 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508618</comments>
            <pubDate>Wed, 31 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508618</guid>        </item>
        <item>
            <title>A prospective open-label trial of lamotrigine monotherapy in children and adolescents with bipolar disorder.</title>
            <link>http://www.medworm.com/index.php?rid=3508617&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20415838%26dopt%3DAbstract</link>
            <description>Conclusions: Open-label lamotrigine treatment appears to be beneficial in the treatment of bipolar disorder and associated conditions in children. Future placebo-controlled, double-blind studies are warranted to confirm these findings.
    PMID: 20415838 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508617</comments>
            <pubDate>Wed, 31 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508617</guid>        </item>
        <item>
            <title>Hyperbaric oxygen therapy for multiple sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=3508616&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20415839%26dopt%3DAbstract</link>
            <description>This article summarizes the clinical evidence for the use of HBO(2)T in the treatment of MS. We conducted a literature review focused on the interaction of hyperbaric oxygenation and MS. In particular, we appraised the clinical data regarding treatment and performed a meta-analysis of the randomized evidence using the methodology of the Cochrane Collaboration. We found 12 randomized studies in the area, all of which were performed between 1983 and 1987. A meta-analysis of this evidence suggests there is no clinically significant benefit from the administration of HBO(2)T. The great majority of randomized trials investigated a course of 20 treatments at pressures between 1.75ATA and 2.5ATA daily for 60-120 min over 4 weeks against a placebo regimen. None have tested the efficacy of HBO(2)T ...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508616</comments>
            <pubDate>Wed, 31 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508616</guid>        </item>
        <item>
            <title>Effects of Acetazolamide on Transient K(+) Currents and Action Potentials in Nodose Ganglion Neurons of Adult Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3450167&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20370806%26dopt%3DAbstract</link>
            <description>Authors: Matsumoto S, Yoshida S, Ikeda M, Kadoi J, Takahashi M, Tanimoto T, Kitagawa J, Saiki C, Takeda M, Shima Y
    The aim of the present study was to determine whether acetazolamide (AZ) contributes to the inhibition of the fast inactivating transient K(+) current (I(A)) in adult rat nodose ganglion (NG) neurons. We have previously shown that pretreatment with either AZ or 4-AP attenuated or blocked the CO(2)-induced inhibition of slowly adapting pulmonary stretch receptors in in vivo experiments. The patch-clamp experiments were performed by using the isolated NG neurons. In addition to this, the RT-PCR of mRNA and the expression of voltage-gated K(+) (Kv) 1.4, Kv 4.1, Kv 4.2, and Kv 4.3 channel proteins from nodose ganglia were examined. We used NG neurons sensitive to the 1 mM AZ a...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3450167</comments>
            <pubDate>Tue, 30 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3450167</guid>        </item>
        <item>
            <title>Ataques de Nervios and Somatic Complaints Among Island and Mainland Puerto Rican Children.</title>
            <link>http://www.medworm.com/index.php?rid=3450171&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20370802%26dopt%3DAbstract</link>
            <description>In this study, we assessed the relation between this anxiety-related experience, henceforth ataques, and somatic complaints in a probability sample of Puerto Rican youth, ages 5-13 years, living in San Juan, Puerto Rico (N = 1353) and in the South Bronx, New York (N = 1138). When both sites were combined, children with ataques were significantly more likely to have either a lifetime prevalence of asthma or headaches, and tended to have more stomach aches and a history of epilepsy or seizure than children without ataques. Further within site analyses showed a similar patterning of complaints for the South Bronx sample as for the combined sample. However, children in San Juan with ataques were only slightly more likely to experience headaches, and at risk for injury, than those without ataqu...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3450171</comments>
            <pubDate>Sun, 28 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3450171</guid>        </item>
        <item>
            <title>Association Between Polymorphisms in GRIK2 Gene and Obsessive-Compulsive Disorder: A Family-Based Study.</title>
            <link>http://www.medworm.com/index.php?rid=3450170&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20370803%26dopt%3DAbstract</link>
            <description>This study examines GRIK2 as a candidate gene for OCD susceptibility in a family-based approach. Probands had full DSM-IV diagnostic criteria for OCD. Forty-seven OCD probands and their parents were recruited from tertiary care OCD specialty clinics from France and USA. Genotypes of single nucleotide polymorphism (SNP) markers and related haplotypes were analyzed using Haploview and FBAT software. The polymorphism at rs1556995 (P= 0.0027; permuted P-value = 0.03) was significantly associated with the presence of OCD. Also, the two marker haplotype rs1556995/rs1417182, was significantly associated with OCD (P= 0.0019, permuted P-value = 0.01). This study supports previously reported findings of association between proximal GRIK2 SNPs and OCD in a comprehensive evaluation of the gene. Furthe...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3450170</comments>
            <pubDate>Sun, 28 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3450170</guid>        </item>
        <item>
            <title>Acetylcholine-Dopamine Interactions in the Pathophysiology and Treatment of CNS Disorders.</title>
            <link>http://www.medworm.com/index.php?rid=3450169&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20370804%26dopt%3DAbstract</link>
            <description>Authors: Lester DB, Rogers TD, Blaha CD
    Dopaminergic neurons in the substantia nigra pars compacta and ventral tegmental area of the midbrain form the nigrostriatal and mesocorticolimbic dopaminergic pathways that, respectively, project to dorsal and ventral striatum (including prefrontal cortex). These midbrain dopaminergic nuclei and their respective forebrain and cortical target areas are well established as serving a critical role in mediating voluntary motor control, as evidenced in Parkinson's disease, and incentive-motivated behaviors and cognitive functions, as exhibited in drug addiction and schizophrenia, respectively. Although it cannot be disputed that excitatory and inhibitory amino acid-based neurotransmitters, such as glutamate and GABA, play a vital role in modulating a...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3450169</comments>
            <pubDate>Sun, 28 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3450169</guid>        </item>
        <item>
            <title>Drug Profile: Transdermal Rivastigmine Patch in the Treatment of Alzheimer Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3450168&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20370805%26dopt%3DAbstract</link>
            <description>Authors: Emre M, Bernabei R, Blesa R, Bullock R, Cunha L, Dani&amp;#xEB;ls H, Dziadulewicz E, F&amp;#xF6;rstl H, Fr&amp;#xF6;lich L, Gabryelewicz T, Levin O, Lindesay J, Mart&amp;#xED;nez-Lage P, Monsch A, Tsolaki M, van Laar T
    Cholinesterase inhibitors constitute one of the mainstays of treatment of Alzheimer disease (AD). Gastrointestinal side effects, difficulty accessing therapeutic doses and poor patient compliance have been identified as barriers to effective treatment with these substances. The rivastigmine transdermal patch provides continuous delivery of drug through the skin into the bloodstream, avoiding the fluctuations in plasma concentration associated with oral administration. This pharmacokinetic profile is associated with reduced side effects, resulting in easier access to expected ta...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3450168</comments>
            <pubDate>Sun, 28 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3450168</guid>        </item>
        <item>
            <title>Critical role of Nitric Oxide on Nicotine-Induced Hyperactivation of Dopaminergic Nigrostriatal System: Electrophysiological and Neurochemical evidence in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3421103&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20345972%26dopt%3DAbstract</link>
            <description>In this study, using single cell recordings in vivo coupled with microiontophoresis and microdialysis in freely moving animals, the role of NO signaling on the hyperactivation elicited by nicotine of the nigrostriatal system was investigated in rats. Nicotine induced a dose-dependent increase of the firing activity of the substantia nigra pars compacta (SNc) DA neurons and DA and 3,4-dihydroxyphenylacetic acid (DOPAC) release in the striatum. Pharmacological manipulation of the NO system did not produce any change under basal condition in terms of neuronal discharge and DA release. In contrast, pretreatments with two NO synthase (NOS) inhibitors, N-omega-nitro-l-arginine methyl ester (l-NAME) and 7-nitroindazole (7-NI) were both capable of blocking the nicotine-induced increase of SNc DA n...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3421103</comments>
            <pubDate>Thu, 25 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3421103</guid>        </item>
        <item>
            <title>Apathy Diagnosis, Assessment, and Treatment in Alzheimer's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3421102&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20345973%26dopt%3DAbstract</link>
            <description>Authors: Robert PH, Mulin E, Mall&amp;#xE9;a P, David R
    Apathy is defined as a disorder of motivation. There is wide acknowledgement that apathy is an important behavioral syndrome in Alzheimer's disease and in various neuropsychiatric disorders. In light of recent research and the renewed interest in the correlates and impacts of apathy and in its treatments, it is important to develop criteria for apathy that will be widely accepted, have clear operational steps, and be easy to apply in clinical practice and in research settings. Meeting these needs was the focus for a task force that included members of the European Psychiatric Association, the European Alzheimer's Disease Consortium and experts from Europe, Australia and North America.
    PMID: 20345973 [PubMed - as supplied by publis...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3421102</comments>
            <pubDate>Thu, 25 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3421102</guid>        </item>
        <item>
            <title>Adenosine-Dopamine Interactions in the Pathophysiology and Treatment of CNS Disorders.</title>
            <link>http://www.medworm.com/index.php?rid=3421104&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20345970%26dopt%3DAbstract</link>
            <description>Authors: Fuxe K, Marcellino D, Borroto-Escuela DO, Guescini M, Fern&amp;#xE1;ndez-Due&amp;#xF1;as V, Tanganelli S, Rivera A, Ciruela F, Agnati LF
    Adenosine-dopamine interactions in the central nervous system (CNS) have been studied for many years in view of their relevance for disorders of the CNS and their treatments. The discovery of adenosine and dopamine receptor containing receptor mosaics (RM, higher-order receptor heteromers) in the striatum opened up a new understanding of these interactions. Initial findings indicated the existence of A(2A)R-D(2)R heterodimers and A(1)R-D(1)R heterodimers in the striatum that were followed by indications for the existence of striatal A(2A)R-D(3)R and A(2A)R-D(4)R heterodimers. Of particular interest was the demonstration that antagonistic allosteric A...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3421104</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3421104</guid>        </item>
        <item>
            <title>The Novel Antidepressant Agomelatine Normalizes Hippocampal Neuronal Activity and Promotes Neurogenesis in Chronically Stressed Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3381590&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20236141%26dopt%3DAbstract</link>
            <description>Authors: Dagyt&amp;#x117; G, Trentani A, Postema F, Luiten PG, Den Boer JA, Gabriel C, Moca&amp;#xEB;r E, Meerlo P, Van der Zee EA
    Agomelatine is a novel antidepressant which acts as a melatonergic (MT1/MT2) receptor agonist and serotonergic (5-HT(2C)) receptor antagonist. The antidepressant properties of agomelatine have been demonstrated in animal models as well as in clinical studies. Several preclinical studies reported agomelatine-induced effects on brain plasticity, mainly under basal conditions in healthy animals. Yet, it is important to unravel agomelatine-mediated changes in the brain affected by psychopathology or exposed to conditions that might predispose to mood disorders. Since stress is implicated in the etiology of depression, it is valid to investigate antidepressant-induced e...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3381590</comments>
            <pubDate>Thu, 11 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3381590</guid>        </item>
        <item>
            <title>A Review of the Neural Mechanisms of Action and Clinical Efficiency of Riluzole in Treating Amyotrophic Lateral Sclerosis: What have we Learned in the Last Decade?</title>
            <link>http://www.medworm.com/index.php?rid=3381589&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20236142%26dopt%3DAbstract</link>
            <description>Authors: Bellingham MC
    Amyotrophic lateral sclerosis (ALS) is a devastating and fatal neurodegenerative disease of adults which preferentially attacks the neuromotor system. Riluzole has been used as the only approved treatment for amyotrophic lateral sclerosis since 1995, but its mechanism(s) of action in slowing the progression of this disease remain obscure. Searching PubMed for &quot;riluzole&quot; found 705 articles published between January 1996 and June 2009. A systematic review of this literature found that riluzole had a wide range of effects on factors influencing neural activity in general, and the neuromotor system in particular. These effects occurred over a large dose range (&amp;lt;1 muM to &amp;gt;1 mM). Reported neural effects of riluzole included (in approximate ascending order of dose...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3381589</comments>
            <pubDate>Wed, 10 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3381589</guid>        </item>
        <item>
            <title>Deficits in Psychological Well-Being and Quality-of-Life in Minor Depression: Implications for DSM-V.</title>
            <link>http://www.medworm.com/index.php?rid=3381592&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20236139%26dopt%3DAbstract</link>
            <description>Conclusions: Mild depressive symptoms with Min D are associated with major deficits in QOL and PWB measures of environmental mastery and poor self-acceptance. Our findings suggest that diminished QOL and PWB may be intrinsic cognitive aspects of Min D with or without a history of MDD. It may be unnecessary in the DSM IV-TR to exclude the diagnosis of Min D if a subject has had a past episode of MDD. * Minor depression exists along a continuum of depression. * Deficits in psychological well-being and quality-of-life in minor depression are severe. * No difference in these measures if minor depression existed with or without a history of major depression.
    PMID: 20236139 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3381592</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3381592</guid>        </item>
        <item>
            <title>Insulin-Like Growth Factor -1 (IGF-1) Derived Neuropeptides, a Novel Strategy for the Development of Pharmaceuticals for Managing Ischemic Brain Injury.</title>
            <link>http://www.medworm.com/index.php?rid=3381591&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20236140%26dopt%3DAbstract</link>
            <description>Authors: Guan J
    Insulin-Like Growth Factor-1 (IGF-1) is neuroprotective and improves long-term function after brain injury. However, its clinical application to neurological disorders is limited by its large molecular size, poor central uptake, and mitogenic potential. Glycine-proline-glutamate (GPE) is naturally cleaved from the IGF-1 N-terminal and is also neuroprotective after ischemic injury, thus providing a potential novel strategy of drug discovery for management of neurological disorders. GPE is not enzymatically stable, thus intravenous infusion of GPE becomes necessary for stable and potent neuroprotection. The broad effective dose range and treatment window of 3-7 h after the lesion suggest its potential for treating acute brain injuries. The neuroprotective action of GPE is...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3381591</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3381591</guid>        </item>
        <item>
            <title>Occurrence and treatment of ADHD in adults.</title>
            <link>http://www.medworm.com/index.php?rid=3179269&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20070784%26dopt%3DAbstract</link>
            <description>Authors: Meyer JS
    
    PMID: 20070784 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179269</comments>
            <pubDate>Sun, 17 Jan 2010 00:24:03 +0100</pubDate>
            <guid isPermaLink="false">3179269</guid>        </item>
        <item>
            <title>Nutritional interventions for treatment of seasonal affective disorder.</title>
            <link>http://www.medworm.com/index.php?rid=3179268&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20070785%26dopt%3DAbstract</link>
            <description>Authors: Palinkas LA
    
    PMID: 20070785 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179268</comments>
            <pubDate>Sun, 17 Jan 2010 00:24:03 +0100</pubDate>
            <guid isPermaLink="false">3179268</guid>        </item>
        <item>
            <title>Atomoxetine in the treatment of adults with subthreshold and/or late onset attention-deficit hyperactivity disorder-not otherwise specified (ADHD-NOS): a prospective open-label 6-week study.</title>
            <link>http://www.medworm.com/index.php?rid=3179267&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20070786%26dopt%3DAbstract</link>
            <description>The objective of this study was to evaluate the efficacy and tolerability of atomoxetine hydrochloride (ATX) in the treatment of adults with atypical manifestations of attention-deficit hyperactivity disorder (ADHD) (not otherwise specified [NOS]). We hypothesized that treatment with ATX will be safe and efficacious for the treatment of adults with ADHD-NOS. This was a 6-week, open-label, prospective treatment study of ATX monotherapy in 45 adult patients with ADHD-NOS assessed using standardized instruments for diagnosis and a robust oral daily dose of up to 1.2 mg/kg/day or 120 mg/day. Symptom severity was assessed with the adult ADHD Investigator Symptom Report Scale (AISRS) and Clinical Global Impression Scale. Treatment with ATX at an average daily dose of 78.7 +/- 27.8 mg was associa...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179267</comments>
            <pubDate>Sun, 17 Jan 2010 00:24:03 +0100</pubDate>
            <guid isPermaLink="false">3179267</guid>        </item>
        <item>
            <title>Pregnenolone, dehydroepiandrosterone, and schizophrenia: alterations and clinical trials.</title>
            <link>http://www.medworm.com/index.php?rid=3179266&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20070787%26dopt%3DAbstract</link>
            <description>Authors: Ritsner MS
    Neurosteroids, such as pregnenolone (PREG), dehydroepiandrosterone (DHEA), and their sulfates (PREGS and DHEAS) are reported to have a modulatory effect on neuronal excitability and synaptic plasticity. They also have many other functions associated with neuroprotection, response to stress, mood regulation, and cognitive performance. Furthermore, these neurosteroids have been linked to, and their levels are altered in, neuropsychiatric disorders. This review highlights what is currently known about the metabolism and mode of action of PREG and DHEA, as well as about alterations of these neurosteroids in schizophrenia. This review also provides substantial information about clinical trials with DHEA and PREG augmentation with of antipsychotic agents in schizophrenia....</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179266</comments>
            <pubDate>Sun, 17 Jan 2010 00:24:03 +0100</pubDate>
            <guid isPermaLink="false">3179266</guid>        </item>
        <item>
            <title>Pregabalin in the treatment of alcohol and benzodiazepines dependence.</title>
            <link>http://www.medworm.com/index.php?rid=3179265&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20070788%26dopt%3DAbstract</link>
            <description>Authors: Oulis P, Konstantakopoulos G
    We review all available studies on the use of the newer anticonvulsant drug pregabalin (PGB) in the treatment of both alcohol dependence (AD) and benzodiazepine dependence (BD). In AD, the available evidence includes one open-label and one double-blind randomized studies, whereas in BD, only a few case reports and one open-label study are as yet available. In both conditions, PGB was found efficacious with significant improvement in withdrawal symptoms at the dosage ranges of 150-450 mg/day (AD) and 225-900 mg/day (BD). Moreover, its side effects were mild and transient. Despite the limited quality of the studies design, their findings suggest that PGB might constitute a novel efficacious and safe option in the treatment of both AD and BD.
    PMID...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179265</comments>
            <pubDate>Sun, 17 Jan 2010 00:24:03 +0100</pubDate>
            <guid isPermaLink="false">3179265</guid>        </item>
        <item>
            <title>Switching from oral cholinesterase inhibitors to the rivastigmine transdermal patch.</title>
            <link>http://www.medworm.com/index.php?rid=3179264&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20070789%26dopt%3DAbstract</link>
            <description>The objective of this review was to consider available data from patients switching from oral ChEIs to transdermal rivastigmine treatment, and to suggest practical guidelines for patients wishing to do this. Literature database and reference list searches were performed to identify suitable publications. Data from two clinical trials and a series of open observational studies, in which patients were switched to the rivastigmine patch from oral rivastigmine, donepezil tablets, or galantamine, were evaluated. Adverse events were tabulated. In the studies reported here, nausea was reported in up to 3.2% and vomiting in up to 1.9% of patients switching to the rivastigmine patch from oral rivastigmine. Similar rates (up to 3.8% of patients for nausea and 0.8% of patients for vomiting) were repo...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179264</comments>
            <pubDate>Sun, 17 Jan 2010 00:24:03 +0100</pubDate>
            <guid isPermaLink="false">3179264</guid>        </item>
        <item>
            <title>A Multicenter, Placebo-Controlled, Double-Blind, Randomized Study of Efficacy and Safety of Ocinaplon (DOV 273,547) in Generalized Anxiety Disorder.</title>
            <link>http://www.medworm.com/index.php?rid=3135936&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20041911%26dopt%3DAbstract</link>
            <description>Authors: Czobor P, Skolnick P, Beer B, Lippa A
    Preclinical studies demonstrated that ocinaplon, a positive allosteric modulator of GABA(A) receptors, possesses anxiolytic-like actions at doses devoid of the side effects typically associated with benzodiazepines. The aim of this study was to evaluate the effects of ocinaplon in a multicenter, double-blind proof-of-concept trial of male and female outpatients who met DSM-IV criteria for GAD with no coexisting depression, and had a baseline score of &amp;gt;/=20 on the Hamilton Scale for Anxiety (HAM-A). Patients with &amp;lt;20% reduction in HAM-A to placebo in a single-blind 7-day run-in period were randomly assigned to treatment with ocinaplon 90 mg t.i.d. (n = 31) or placebo for 28 days (n = 29). Ocinaplon was more effective than placebo in r...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3135936</comments>
            <pubDate>Tue, 22 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3135936</guid>        </item>
        <item>
            <title>Is Anticonvulsant Treatment of Mania a Class Effect? Data from Randomized Clinical Trials.</title>
            <link>http://www.medworm.com/index.php?rid=3105666&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015083%26dopt%3DAbstract</link>
            <description>Authors: Rosa AR, Fountoulakis K, Siamouli M, Gonda X, Vieta E
    Our aim was to evaluate the efficacy and tolerability of anticonvulsant agents for the treatment of acute bipolar mania and ascertain if their effects on mania are a &quot;class&quot; effect. We conducted a systematic review of randomized controlled trials (RCTs) with placebo or active comparator, in acute bipolar mania in order to summarize available data on anticonvulsant treatment of mania/mixed episodes. We searched (PubMed/MEDLINE) with the combination of the words &quot;acute mania&quot; and &quot;clinical trials&quot; with each one of the following words: &quot;anticonvulsants/antiepileptics,&quot;&quot;valproic/valproate/divalproex,&quot;&quot;carbamazepine,&quot;&quot;oxcarbazepine,&quot;&quot;lamotrigine,&quot;&quot;gabapentin,&quot;&quot;topiramate,&quot;&quot;phenytoin,&quot;&quot;zonisamide,&quot;&quot;retigabine,&quot;&quot;pregabalin,&quot;&quot;tiaga...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105666</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105666</guid>        </item>
        <item>
            <title>TGF-beta1 Pathway as a New Target for Neuroprotection in Alzheimer's Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3015879&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19925479%26dopt%3DAbstract</link>
            <description>Authors: Caraci F, Battaglia G, Bruno V, Bosco P, Carbonaro V, Giuffrida ML, Drago F, Sortino MA, Nicoletti F, Copani A
    Alzheimer's disease (AD) is a neurodegenerative disorder that affects more than 37 million people worldwide. Current drugs for AD are only symptomatic, but do not interfere with the underlying pathogenic mechanisms of the disease. AD is characterized by the presence of ss-amyloid (Abeta) plaques, neurofibrillary tangles, and neuronal loss. The identification of the molecular determinants underlying AD pathogenesis is a fundamental step to design new disease-modifying drugs. Recently, a specific impairment of transforming-growth-factor-beta1 (TGF-beta1) signaling pathway has been demonstrated in AD brain. The deficiency of TGF-beta1 signaling has been shown to increase...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3015879</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3015879</guid>        </item>
        <item>
            <title>Dopamine, Morphine, and Nitric Oxide: An Evolutionary Signaling Triad.</title>
            <link>http://www.medworm.com/index.php?rid=3003521&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19912274%26dopt%3DAbstract</link>
            <description>Authors: Stefano GB, Kream RM
    Morphine biosynthesis in relatively simple and complex integrated animal systems has been demonstrated. Key enzymes in the biosynthetic pathway have also been identified, that is, CYP2D6 and COMT. Endogenous morphine appears to exert highly selective actions via novel mu opiate receptor subtypes, that is, mu3,-4, which are coupled to constitutive nitric oxide release, exerting general yet specific down regulatory actions in various animal tissues. The pivotal role of dopamine as a chemical intermediate in the morphine biosynthetic pathway in plants establishes a functional basis for its expansion into an essential role as the progenitor catecholamine signaling molecule underlying neural and neuroendocrine transmission across diverse animal phyla. In invert...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3003521</comments>
            <pubDate>Fri, 13 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3003521</guid>        </item>
        <item>
            <title>Cognitive deficits in bipolar individuals: implications for clinical practice.</title>
            <link>http://www.medworm.com/index.php?rid=2968631&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19889127%26dopt%3DAbstract</link>
            <description>Authors: Friedman ES
    
    PMID: 19889127 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2968631</comments>
            <pubDate>Sat, 07 Nov 2009 13:52:05 +0100</pubDate>
            <guid isPermaLink="false">2968631</guid>        </item>
        <item>
            <title>Answers and questions: a star*D report.</title>
            <link>http://www.medworm.com/index.php?rid=2968630&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19889128%26dopt%3DAbstract</link>
            <description>Authors: Osher Y
    
    PMID: 19889128 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2968630</comments>
            <pubDate>Sat, 07 Nov 2009 13:52:05 +0100</pubDate>
            <guid isPermaLink="false">2968630</guid>        </item>
        <item>
            <title>Galantamine-ER for cognitive dysfunction in bipolar disorder and correlation with hippocampal neuronal viability: a proof-of-concept study.</title>
            <link>http://www.medworm.com/index.php?rid=2968629&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19889129%26dopt%3DAbstract</link>
            <description>CONCLUSION: Bipolar subjects had cognitive dysfunction; treatment with Galantamine-ER was associated with improved cognition and with increases in neuronal viability and normalization of lipid membrane metabolism in the left hippocampus. This study was registered on ClinicalTrials.gov (NCT00181636).
    PMID: 19889129 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2968629</comments>
            <pubDate>Sat, 07 Nov 2009 13:52:05 +0100</pubDate>
            <guid isPermaLink="false">2968629</guid>        </item>
        <item>
            <title>Potential mechanisms involved in the prevention of neurodegenerative diseases by lithium.</title>
            <link>http://www.medworm.com/index.php?rid=2968623&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19889130%26dopt%3DAbstract</link>
            <description>Authors: Camins A, Verdaguer E, Junyent F, Yeste-Velasco M, Pelegr&amp;#xED; C, Vilaplana J, Pall&amp;#xE1;s M
    Lithium is a monovalent cation that was introduced in 1949 by John Cade for the treatment of bipolar disorder. Clinical reports and subsequent studies confirmed this application and the beneficial effects of this compound. However, over the last 15 years, various authors have also demonstrated the neuroprotective effects of lithium against several neurotoxic paradigms. Thus, experimental studies in neuronal cell cultures and animal models of Alzheimer disease and others pathologies have provided strong evidence for the potential benefits of lithium. The main mechanism underlying its neuroprotective effects is thought to be inhibition of glycogen synthase kinase-3 (GSK-3), although oth...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2968623</comments>
            <pubDate>Sat, 07 Nov 2009 13:52:05 +0100</pubDate>
            <guid isPermaLink="false">2968623</guid>        </item>
        <item>
            <title>Biological Marker Candidates of Alzheimer's Disease in Blood, Plasma, and Serum.</title>
            <link>http://www.medworm.com/index.php?rid=2912913&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19840034%26dopt%3DAbstract</link>
            <description>Authors: Schneider P, Hampel H, Buerger K
    At the earliest clinical stages of Alzheimer's disease (AD), when first symptoms are mild, making a reliable and accurate diagnosis is difficult. AD related brain pathology and underlying molecular mechanisms precede symptoms. Biological markers can serve as supportive early screening and diagnostic tools as well as indicators of presymptomatic biochemical change. Moreover, biomarkers cover a variety of roles and functions such as disease prediction, indicating disease acuity and progression, and may ensure biological mapping of treatment outcome. Early screening, detection, and diagnosis of AD would permit earlier disease modifying intervention at potentially reversible stages. To date, most established biological markers from both cerebrospin...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912913</comments>
            <pubDate>Tue, 13 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912913</guid>        </item>
        <item>
            <title>The Antiapoptotic Activity of Melatonin in Neurodegenerative Diseases.</title>
            <link>http://www.medworm.com/index.php?rid=2887969&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818070%26dopt%3DAbstract</link>
            <description>Authors: Wang X
    Melatonin plays a neuroprotective role in models of neurodegenerative diseases. However, the molecular mechanisms underlying neuroprotection by melatonin are not well understood. Apoptotic cell death in the central nervous system is a feature of neurodegenerative diseases. The intrinsic and extrinsic apoptotic pathways and the antiapoptotic survival signal pathways play critical roles in neurodegeneration. This review summarizes the reports to date showing inhibition by melatonin of the intrinsic apoptotic pathways in neurodegenerative diseases including stroke, Alzheimer disease, Parkinson disease, Huntington disease, and amyotrophic lateral sclerosis. Furthermore, the activation of survival signal pathways by melatonin in neurodegenerative diseases is discussed.
    P...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887969</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887969</guid>        </item>
        <item>
            <title>Lomerizine, a Ca(2+) Channel Blocker, Protects against Neuronal Degeneration within the Visual Center of the Brain after Retinal Damage in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2847426&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19788586%26dopt%3DAbstract</link>
            <description>Authors: Ito Y, Nakamura S, Tanaka H, Tsuruma K, Shimazawa M, Araie M, Hara H
    The purpose of this study was to determine whether lomerizine, a Ca(2+) channel blocker, protects against neuronal degeneration within the dorsal lateral geniculate nucleus (dLGN) and superior colliculus (SC) after the induction of retinal damage by intravitreal injection of N-methyl-D-aspartate (NMDA) in mice. NMDA (20 mM/2 muL) was injected into the vitreous body of the left eye in mice (DAY 0). Lomerizine at 30 mg/kg, p.o. was administered daily from immediately after the injection of NMDA (DAY 0) to 90 days after (DAY 90). To investigate the neuroprotective effects of lomerizine, the retina, dLGN, and SC were examined using histochemistry and immunohistochemistry. Lomerizine reduced the retinal damage ind...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847426</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847426</guid>        </item>
        <item>
            <title>Report of Two Double-Blind Randomized Placebo-Controlled Pilot Studies of a Carbohydrate-Rich Nutrient Mixture for Treatment of Seasonal Affective Disorder (SAD).</title>
            <link>http://www.medworm.com/index.php?rid=2824903&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19769596%26dopt%3DAbstract</link>
            <description>Authors: Mischoulon D, Pedrelli P, Wurtman J, Vangel M, Wurtman R
    We investigated a carbohydrate-rich nutrient-drink mix for treatment of seasonal affective disorder (SAD). This mixture may contribute to brain serotonin synthesis, potentially exerting an antidepressant effect and controlling carbohydrate cravings. Two successive double-blind placebo-controlled studies were performed. In Study 1, 18 subjects (50% women; mean age 43 +/- 15 years) with SCID-diagnosed SAD were randomized to 12 days of twice daily carbohydrate beverage (CHO) containing mixed starches, or a placebo beverage (PRO) containing the CHO mix plus casein protein to dampen serotonin synthesis. Following a 2-day washout, subjects were crossed over to the other treatment for 12 days. In Study 2, 32 subjects (63% women...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2824903</comments>
            <pubDate>Sun, 20 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2824903</guid>        </item>
        <item>
            <title>Neurological and Cardiovascular Adverse Events Associated with Antimanic Treatment in Children and Adolescents.</title>
            <link>http://www.medworm.com/index.php?rid=2824902&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19769597%26dopt%3DAbstract</link>
            <description>Authors: Jerrell JM
    To identify the factors associated with incident neurological and cardiovascular adverse events in children and adolescents treated with antimanic agents, a retrospective, longitudinal study was conducted. Medicaid medical and pharmacy claims between January 1996 and December 2005 were used to identify 3657 children and adolescents prescribed antimanic medications, and a random sample of 4500 children not treated with psychotropic medications. All adverse events examined (sedation/drowsiness, headaches, involuntary movements/extrapyramidal symptoms (EPS), cardiovascular events, hypertension, and orthostatic hypotension) were more prevalent in the antimanic-treated cohort. The odds of developing incident sedation/drowsiness and headaches were significantly higher for...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2824902</comments>
            <pubDate>Sun, 20 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2824902</guid>        </item>
        <item>
            <title>Neuroendocrine-Related Adverse Events Associated with Antidepressant Treatment in Children and Adolescents.</title>
            <link>http://www.medworm.com/index.php?rid=2824901&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19769598%26dopt%3DAbstract</link>
            <description>This study identifies the factors associated with incident neuroendocrine-related metabolic, digestive, and sexual/reproductive adverse events in children and adolescents treated with antidepressants. A retrospective cohort design evaluating Medicaid medical and pharmacy claims between January, 1996 and December, 2005 was employed for 11970 children and adolescents prescribed an antidepressant medication, and a random sample of 4500 children not treated with psychotropic medications. Incident obesity/weight gain, Type 2 diabetes mellitus, and dyslipidemia were more likely for those prescribed selective serotonin reuptake inhibitors (SSRIs) (OR = 1.49; 1.37; 1.44), whereas Type 2 diabetes mellitus and dyslipidemia were more likely for those prescribed weight-inducing antidepressants (ORs = ...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2824901</comments>
            <pubDate>Sun, 20 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2824901</guid>        </item>
        <item>
            <title>Validation of the Massachusetts General Hospital Antidepressant Treatment History Questionnaire (ATRQ).</title>
            <link>http://www.medworm.com/index.php?rid=2824900&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19769599%26dopt%3DAbstract</link>
            <description>Authors: Chandler GM, Iosifescu DV, Pollack MH, Targum SD, Fava M
    The low rate of response to antidepressants in treatment resistant depression (TRD) justifies studies of next-step therapies following a treatment failure. In TRD clinical trials, it is important to verify the accurate diagnosis of treatment resistance for all enrolled subjects using a reliable and valid instrument. Self-rated scales can reduce the impact of investigator bias and reduce the time burden for clinical researchers. The Massachusetts General Hospital (MGH) Antidepressant Treatment Response Questionnaire (ATRQ) is a self-rated scale used to determine treatment resistance in major depressive disorder (MDD). The ADAPT-A study is a multi-center double-blind, placebo-controlled study of low-dose aripiprazole adjun...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2824900</comments>
            <pubDate>Sun, 20 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2824900</guid>        </item>
        <item>
            <title>The Impact of Nonclinical Factors on Care Use for Patients with Depression: A STAR*D Report.</title>
            <link>http://www.medworm.com/index.php?rid=2745900&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19712127%26dopt%3DAbstract</link>
            <description>Conclusions: Data suggest diligent, measurement-based mental health programs may reduce race, gender, and education disparities in the use of needed mental health care.
    PMID: 19712127 [PubMed - as supplied by publisher] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2745900</comments>
            <pubDate>Wed, 26 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2745900</guid>        </item>
        <item>
            <title>Introduction to the special issue: anxiety disorders in cross-cultural perspective.</title>
            <link>http://www.medworm.com/index.php?rid=2720979&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19691539%26dopt%3DAbstract</link>
            <description>Authors: Hinton DE, Pollack MH
    This special issue explores the cross-cultural variation in the presentation and generation of anxiety disorders. As a background review, in this Introduction, we illustrate how the cognitive theory of the generation of anxiety disorders explains how such cross-cultural variation occurs. We first show how the &quot;catastrophic cognitions&quot; theory applies to panic disorder and then suggest how the &quot;catastrophic cognitions&quot; theory applies to all anxiety disorders-and so explains the existence of profound cultural influence on the presentation and generation of the anxiety disorders.
    PMID: 19691539 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2720979</comments>
            <pubDate>Sat, 22 Aug 2009 00:52:02 +0100</pubDate>
            <guid isPermaLink="false">2720979</guid>        </item>
        <item>
            <title>Lives in Isolation: stories and struggles of low-income African American women with panic disorder.</title>
            <link>http://www.medworm.com/index.php?rid=2720978&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19691540%26dopt%3DAbstract</link>
            <description>Authors: Johnson M, Mills TL, Deleon JM, Hartzema AG, Haddad J
    Research evidence points to the existence of racial-ethnic disparities in both access to and quality of mental health services for African Americans with panic disorder. Current panic disorder evaluation and treatment paradigms are not responsive to the needs of many African Americans. The primary individual, social, and health-care system factors that limit African Americans' access to care and response to treatment are not well understood. Low-income African American women with panic disorder participated in a series of focus-group sessions designed to elicit (1) their perspectives regarding access and treatment barriers and (2) their recommendations for designing a culturally consistent panic treatment program. Fear of c...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
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            <pubDate>Sat, 22 Aug 2009 00:52:02 +0100</pubDate>
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        <item>
            <title>The assessment of the phenomenology of sleep paralysis: the Unusual Sleep Experiences Questionnaire (USEQ).</title>
            <link>http://www.medworm.com/index.php?rid=2720977&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19691541%26dopt%3DAbstract</link>
            <description>Authors: Paradis C, Friedman S, Hinton DE, McNally RJ, Solomon LZ, Lyons KA
    Previous research has found a relationship between sleep paralysis (SP) and anxiety states and higher rates have been reported among certain ethnic groups. To advance the cross-cultural study of SP, we developed a brief assessment instrument (which can be self-administered), the Unusual Sleep Experiences Questionnaire (USEQ). In this article, we report on a pilot study with the USEQ in a sample of 208 college students. The instrument was easily understood by the participants, with one quarter reporting at least one lifetime episode of SP. As in previous studies, SP was associated with anxiety (in particular, panic attacks).
    PMID: 19691541 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2720977</comments>
            <pubDate>Sat, 22 Aug 2009 00:52:02 +0100</pubDate>
            <guid isPermaLink="false">2720977</guid>        </item>
        <item>
            <title>Fear of cultural extinction and psychopathology among mandaean refugees: an exploratory path analysis.</title>
            <link>http://www.medworm.com/index.php?rid=2720976&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19691542%26dopt%3DAbstract</link>
            <description>This study aimed to examine the relationships between life experiences, psychopathology and fear of cultural extinction in Mandaean refugees. A survey was conducted of 315 adult Iraqi Mandaean refugees living in Australia. Past traumatic experiences and current resettlement difficulties were assessed. Mental health outcomes were also examined, including measures of posttraumatic stress disorder (PTSD) and depression. Fear of cultural extinction was measured by items developed in consultation with the Mandaean community. A path analysis was employed to investigate the relationship between trauma, living difficulties, PTSD, depression, and fear of cultural extinction. Results indicated that trauma and living difficulties impacted indirectly on fear of cultural extinction, while PTSD (and not...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2720976</comments>
            <pubDate>Sat, 22 Aug 2009 00:52:02 +0100</pubDate>
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        <item>
            <title>Gender and anxiety in Nepal: the role of social support, stressful life events, and structural violence.</title>
            <link>http://www.medworm.com/index.php?rid=2720975&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19691543%26dopt%3DAbstract</link>
            <description>CONCLUSION: Women are at a greater risk of anxiety in Nepal. Social support moderates the risk of anxiety among men but not among women. Ethnography and mixed-methods research are needed to identify other forms of support that may be protective for women and such factors should be promoted in gender-focused mental health interventions.
    PMID: 19691543 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2720975</comments>
            <pubDate>Sat, 22 Aug 2009 00:52:02 +0100</pubDate>
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        <item>
            <title>Panic disorder, panic attacks and panic attack symptoms across race-ethnic groups: results of the collaborative psychiatric epidemiology studies.</title>
            <link>http://www.medworm.com/index.php?rid=2720974&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19691544%26dopt%3DAbstract</link>
            <description>Authors: Asnaani A, Gutner CA, Hinton DE, Hofmann SG
    The current study investigates race-ethnic differences in rates of panic disorder, panic attacks and certain panic attack symptoms by jointly combining three major national epidemiological databases. The compared groups were White, African American, Latino and Asian. The White group had significantly higher rates of panic disorder, and of many panic symptoms, including palpitations, as compared to the African American, Asian and Latino groups. Several expected race-ethnic differences were not found. An explanation for these findings are adduced, and suggestions are given for future studies so that possible ethnic-racial differences in panic disorder, panic attacks and panic attack symptoms can be investigated in a more rigorous manne...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2720974</comments>
            <pubDate>Sat, 22 Aug 2009 00:52:02 +0100</pubDate>
            <guid isPermaLink="false">2720974</guid>        </item>
        <item>
            <title>Mechanisms of efficacy of CBT for Cambodian refugees with PTSD: improvement in emotion regulation and orthostatic blood pressure response.</title>
            <link>http://www.medworm.com/index.php?rid=2720973&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19691545%26dopt%3DAbstract</link>
            <description>Authors: Hinton DE, Hofmann SG, Pollack MH, Otto MW
    Based on the results of a randomized controlled trial, we examined a model of the mechanisms of efficacy of culturally adapted cognitive-behavior therapy (CBT) for Cambodian refugees with pharmacology-resistant posttraumatic stress disorder (PTSD) and comordid orthostatic panic attacks (PAs). Twelve patients were in the initial treatment condition, 12 in the delayed treatment condition. The patients randomized to CBT had much greater improvement than patients in the waitlist condition on all psychometric measures and on one physiological measure-the systolic blood pressure response to orthostasis (d = 1.31)-as evaluated by repeated-measures MANOVA and planned contrasts. After receiving CBT, the Delayed Treatment Group improved on all ...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2720973</comments>
            <pubDate>Sat, 22 Aug 2009 00:52:02 +0100</pubDate>
            <guid isPermaLink="false">2720973</guid>        </item>
        <item>
            <title>A model of the generation of ataque de nervios: the role of fear of negative affect and fear of arousal symptoms.</title>
            <link>http://www.medworm.com/index.php?rid=2720972&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19691546%26dopt%3DAbstract</link>
            <description>This article examines a model of the generation of ataque de nervios, according to which both fear of negative affectivity and fear of arousal symptoms are associated with the emergence of ataques. We examine the relationship of fear of negative affectivity and fear of arousal to the severity of ataque de nervios during the last month and the last 6 months among Caribbean Latinos residing in the United States. The measures include a Fear of Anger Scale and the Anxiety Sensitivity Index (ASI), the ASI augmented with two items that assess fear of arousal symptoms common in ataques: chest tightness and a sense of inner heat. In keeping with the model of ataque generation, one-way analysis of variances (ANOVAs) and discriminant function analyses illustrated that items assessing &quot;fear of negati...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2720972</comments>
            <pubDate>Sat, 22 Aug 2009 00:52:02 +0100</pubDate>
            <guid isPermaLink="false">2720972</guid>        </item>
        <item>
            <title>Symptom dimensions in chinese patients with obsessive-compulsive disorder.</title>
            <link>http://www.medworm.com/index.php?rid=2720971&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19691547%26dopt%3DAbstract</link>
            <description>Authors: Li Y, Marques L, Hinton DE, Wang Y, Xiao ZP
    To study the symptom dimensions of Chinese patients with obsessive-compulsive disorder (OCD), the symptom checklist of the Dimensional Yale-Brown Obsessive-Compulsive Scale (DY-BOCS) was used to assess the symptom dimensions of 139 OCD patients at a mental health center in Shanghai. The most common symptom dimensions were symmetry (67.6%), contamination (43.2%), and aggression (31.7%). The frequency of patients with the miscellaneous, sexual/religious, and hoarding symptom dimensions was 25.9%, 10.8%, and 8.6%, respectively. The frequency of male patients with symmetry concerns was higher than that of the female patients, and the frequency of female patients with contamination concerns was higher than that of male patients. OCD sympt...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2720971</comments>
            <pubDate>Sat, 22 Aug 2009 00:52:02 +0100</pubDate>
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        <item>
            <title>Biological variations in depression and anxiety between East and west.</title>
            <link>http://www.medworm.com/index.php?rid=2720970&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19691548%26dopt%3DAbstract</link>
            <description>This article focuses on the impact of such variations on the diagnosis and treatment of depression and anxiety disorders between East and West. Genes controlling the expression of drug metabolizing enzymes as well as the function of the brain are highly polymorphic, and the patterns and distribution of these polymorphisms are typically divergent across ethnic groups. To the extent that these genetic patterns determine drug response, ethnic variations in these genetic dispositions will lead to differential responses in clinical settings. In addition, the expression of these genes is significantly influenced by environmental factors including diet as well as exposure to other natural products. Superimposed on these biological influences, culturally determined beliefs and behavioral patterns ...</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2720970</comments>
            <pubDate>Sat, 22 Aug 2009 00:52:02 +0100</pubDate>
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        <item>
            <title>Anxiety disorder presentations in asian populations: a review.</title>
            <link>http://www.medworm.com/index.php?rid=2720969&amp;cid=s_37274_168_f&amp;fid=37274&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19691549%26dopt%3DAbstract</link>
            <description>This article reviews typical anxiety presentations in Asia, and among Asian refugees. In Asia, there are multiple functional somatic syndromes that are common anxiety presentations. These distress syndromes often produce catastrophic cognitions about anxiety-type somatic and psychological symptoms. These functional somatic syndromes should be understood, and specifically assessed and addressed, in order to optimize the evaluation and treatment of anxiety disorders among Asian individuals.
    PMID: 19691549 [PubMed - in process] (Source: CNS Neuroscience and Therapeutics)</description>
            <author>CNS Neuroscience and Therapeutics</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2720969</comments>
            <pubDate>Sat, 22 Aug 2009 00:52:02 +0100</pubDate>
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