Journal of Neuroinflammation via MedWorm.com 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 'Journal of Neuroinflammation' source. Wed, 08 Feb 2012 20:43:15 +0100 Functional analysis of Pro-inflammatory properties within the cerebrospinal fluid after subarachnoid hemorrhage in vivo and in vitro http://www.medworm.com/index.php?rid=5668651&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F28 Conclusion: We functionally characterized inflammatory and vasoactive properties of patients' CSF after SAH in vivo and in vitro. This pro-inflammatory milieu in the subarachnoid space might play a pivotal role in the pathophysiology of early and delayed brain injury as well as vasospasm development following SAH. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5668651 Wed, 08 Feb 2012 05:00:00 +0100 5668651 DQB1*0602 rather than DRB1*1501 confers susceptibility to multiple sclerosis-like disease induced by proteolipid protein (PLP) http://www.medworm.com/index.php?rid=5668650&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F29 Conclusions: While genome studies map a strong MS susceptibility effect to the region of DRB1*1501, our findings offer a rationale for potential involvement of pathogenic DQ6-associated autoimmunity in MS. Moreover, that DQB1*0602, but not DRB1*1501, determines disease-susceptibility to PLP in HLA-transgenics, suggests a potential differential, functional role for DQB1*0602 as a predisposing allele in MS. This, together with previously demonstrated disease-susceptibility to MBP and MOG in DRB1*1501-transgenics, also suggests a differential role for DRB1*1501 and DQB1*0602 depending on target antigen and imply a potential complex 'genotype/target antigen/phenotype' relationship in MS heterogeneity. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5668650 Wed, 08 Feb 2012 05:00:00 +0100 5668650 Neuroprotective function for ramified microglia in hippocampal excitotoxicity http://www.medworm.com/index.php?rid=5649989&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F27 Conclusions: Our data strongly suggest that ramified microglia not only screen their microenvironment but additionally protect hippocampal neurons under pathological conditions. Morphological activation of ramified microglia is thus not required to influence neuronal survival. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5649989 Tue, 31 Jan 2012 05:00:00 +0100 5649989 A functional variant in promoter region of platelet-derived growth factor-D is probably associated with intracerebral hemorrhage http://www.medworm.com/index.php?rid=5649990&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F26 Conclusions The -858AA genotype is probably associated with risk for non-hypertensive ICH. Further studies should be conducted to reveal the role of PDGF-D at various stages of ICH development--beneficial, or deleterious. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5649990 Mon, 30 Jan 2012 05:00:00 +0100 5649990 Electroacupuncture pretreatment attenuates cerebral ischemic injury through alpha7 nicotinic acetylcholine receptor-mediated inhibition of high-mobility group box 1 release in rats http://www.medworm.com/index.php?rid=5630476&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F24 Conclusion These data demonstrate that EA pretreatment strongly protects the brain against transient cerebral ischemic injury, and inhibits HMGB1 release through alpha7nAChR activation in rats. These findings suggest the novel potential for stroke interventions harnessing the anti-inflammatory effects of alpha7nAChR activation, through acupuncture or pharmacological strategies. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5630476 Thu, 26 Jan 2012 05:00:00 +0100 5630476 Exacerbation of experimental autoimmune encephalomyelitis in prion protein (PrPc)-null mice: evidence for a critical role of the central nervous system http://www.medworm.com/index.php?rid=5630475&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F25 Conclusions: In view of the present data, it can be concluded that the origin of EAE exacerbation in PrPc-ablated mice resides in the absence of the prion protein in the CNS. Furthermore, the absence of PrPc on both neural and immune cells does not synergize for disease worsening. These conclusions highlight the critical role of PrPc in maintaining the integrity of the CNS in situations of stress, especially during a neuroinflammatory insult. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5630475 Thu, 26 Jan 2012 05:00:00 +0100 5630475 TNF-alpha protein synthesis inhibitor restores neuronal function and reverses cognitive deficits induced by chronic neuroinflammation http://www.medworm.com/index.php?rid=5630477&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F23 Conclusion: Our data demonstrate that the TNF-alpha synthesis inhibitor DT can significantly reverse hippocampus-dependent cognitive deficits induced by chronic neuroinflammation. These results suggest that TNF-alpha is a critical mediator of chronic neuroinflammation-induced neuronal dysfunction and cognitive impairment and targeting its synthesis could provide an effective therapeutic approach to several human neurodegenerative diseases. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5630477 Wed, 25 Jan 2012 05:00:00 +0100 5630477 Concurrent multiple sclerosis and amyotrophic lateral sclerosis: where inflammation and neurodegeneration meet? http://www.medworm.com/index.php?rid=5630480&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F20 The concurrence of multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS) is exceedingly rare and the pathological features have not been examined extensively. Here we describe the key pathological features of a 40 year old man with pathologically confirmed concurrent MS and ALS.This is the most pathologically illustrative case of coincident MS and ALS demonstrating inflammatory and neurodegenerative features characteristic of each disease, and is the first to exhibit the presence of TDP-43 inclusions in this clinical entity. The intricate relationship between neuroinflammation and neurodegeneration in these diseases is discussed. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5630480 Tue, 24 Jan 2012 05:00:00 +0100 5630480 Sequence variants of interleukin 6 (IL-6) are significantly associated with a decreased risk of late-onset Alzheimer's disease http://www.medworm.com/index.php?rid=5630479&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F21 Conclusions: IL-6 polymorphisms are associated with reduced risk of LOAD, especially in ApoE e4 non-carriers. This study identified genetic markers for predicting LOAD in ApoE e4 non-carriers. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5630479 Tue, 24 Jan 2012 05:00:00 +0100 5630479 Selective targeting of microglia by quantum dots http://www.medworm.com/index.php?rid=5630478&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F22 Conclusions: These findings demonstrate that QDs can be used to specifically label and modulate microglia in primary cortical cultures and in brain and may allow for the selective delivery of therapeutic agents to these cells. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5630478 Tue, 24 Jan 2012 05:00:00 +0100 5630478 Neutrophil depletion reduces edema formation and tissue loss following traumatic brain injury in mice http://www.medworm.com/index.php?rid=5621231&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F17 Conclusion: Our results suggest that neutrophils are involved in the edema formation, but not the extravasation of large proteins, as well as contributing to cell death and tissue loss following TBI in mice. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5621231 Mon, 23 Jan 2012 05:00:00 +0100 5621231 CXCL1 can be regulated by IL-6 and promotes granulocyte adhesion to brain capillaries during bacterial toxin exposure and encephalomyelitis http://www.medworm.com/index.php?rid=5621230&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F18 Conclusions: This study identifies CXCL1 not only as a key regulator of granulocyte recruitment into the CNS, but also as a new potential target for the treatment of neuroinflammatory diseases such as multiple sclerosis. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5621230 Mon, 23 Jan 2012 05:00:00 +0100 5621230 Correction: Increased neuroinflammatory and arachidonic acid cascade markers, and reduced synaptic proteins, in brain of HIV-1 transgenic rats. http://www.medworm.com/index.php?rid=5621229&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F19 Correction to Rao J S, Kim H W, Kellom M, Greenstein D, Chen M, Kraft A D, Harry G J, Rapoport S I, Basselin M. Increased neuroinflammatory and arachidonic acid cascade markers, and reduced synaptic proteins, in brain of HIV-1 transgenic rats. Journal of Neuroinflammation 8:101. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5621229 Mon, 23 Jan 2012 05:00:00 +0100 5621229 Constitutive activity of NF-kappa B in myeloid cells drives pathogenicity of monocytes and macrophages during autoimmune neuroinflammation http://www.medworm.com/index.php?rid=5610982&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F15 The NF-kappaB/REL-family of transcription factors plays a central role in coordinating the expression of a wide variety of genes controlling immune responses including autoimmunity of the central nervous system (CNS). The inactive form of NF-kappaB consists of a heterodimer which is complexed with its inhibitor, IkappaB. Conditional knockout-mice for IkappaB in myeloid cells (lysMCreIkappaBfl/fl) have been generated and are characterized by a constitutive activation of NF-kappaB proteins allowing the study of this transcription factor in myelin-oligodendrocyte-glycoprotein induced experimental autoimmune encephalomyelitis (MOG-EAE), a well established experimental model for autoimmune demyelination of the CNS.In comparison to controls, lysMCreIkappaBfl/fl mice developed a more severe clini... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5610982 Fri, 20 Jan 2012 05:00:00 +0100 5610982 Activation of TRPV1 by capsaicin induces functional Kinin B1 receptor in rat spinal cord microglia http://www.medworm.com/index.php?rid=5610981&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F16 Conclusion: This study highlights a new mechanism for B1R induction via TRPV1 activation and establishes a link between these two pro-nociceptive receptors in inflammatory pain. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5610981 Fri, 20 Jan 2012 05:00:00 +0100 5610981 Systemic administration of urocortin after intracerebral hemorrhage reduces neurological deficits and neuroinflammation in rats http://www.medworm.com/index.php?rid=5610984&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F13 Conclusion: Systemic post-ICH treatment with UCN reduces striatal injury and neurological deficits, likely via suppression of microglial activation and inflammatory cytokine production. The low dose of UCN necessary and the clinically amenable peripheral route make UCN a potential candidate for development into a clinical treatment regimen. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5610984 Thu, 19 Jan 2012 05:00:00 +0100 5610984 Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: A multicentre study of 175 patients. http://www.medworm.com/index.php?rid=5610983&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F14 Background: The diagnostic and pathophysiological relevance of antibodies to aquaporin-4 (AQP4-Ab) in patients with neuromyelitis optica spectrum disorders (NMOSD) has been intensively studied. However, little is known so far about the clinical impact of AQP4-Ab seropositivity. Objective: To analyse systematically the clinical and paraclinical features associated with NMO spectrum disorders in Caucasians in a stratified fashion according to the patients' AQP4-Ab serostatus. Methods: Retrospective study of 175 Caucasian patients (AQP4-Ab positive in 78.3%). Results: Seropositive patients were found to be predominantly female (p (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5610983 Thu, 19 Jan 2012 05:00:00 +0100 5610983 Japanese encephalitis virus induces matrix metalloproteinase-9 expression via a ROS/c-Src/PDGFR/PI3K/Akt/MAPKs-dependent AP-1 pathway in rat brain astrocytes http://www.medworm.com/index.php?rid=5599321&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F12 Conclusion: From these results, we conclude that JEV activates the ROS/c Src/PDGFR/PI3K/Akt/MAPKs pathway, which in turn triggers AP-1 activation and ultimately induces MMP-9 expression in RBA-1 cells. These findings concerning JEV-induced MMP-9 expression in RBA-1 cells imply that JEV might play an important role in CNS inflammation and diseases. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5599321 Wed, 18 Jan 2012 01:54:48 +0100 5599321 Eosinophils in glioblastoma biology http://www.medworm.com/index.php?rid=5599322&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F11 Glioblastoma multiforme (GBM) is the most common primary brain tumor in adults. The development of this malignant glial lesion involves a multi-faceted process that results in a loss of genetic or epigenetic gene control, un-regulated cell growth, and immune tolerance. Of interest, atopic diseases are characterized by a lack of immune tolerance and are inversely associated with glioma risk. One cell type that is an established effector cell in the pathobiology of atopic disease is the eosinophil. In response to various stimuli, the eosinophil is able to produce cytotoxic granules, neuromediators, and pro-inflammatory cytokines as well as pro-fibrotic and angiogenic factors involved in pathogen clearance and tissue remodeling and repair. These various biological properties reveal that the e... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5599322 Tue, 17 Jan 2012 05:00:00 +0100 5599322 IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci http://www.medworm.com/index.php?rid=5599326&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F7 Conclusions: Alterations in distribution and composition of CNS inflammatory foci are not sufficient for the onset of atypical EAE. IFNg dictates the course of neuroinflammatory disorders mainly through actions exerted within the CNS. This study provides strong evidence that link microglial STAT1 inactivation to vestibular dysfunction. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5599326 Mon, 16 Jan 2012 05:00:00 +0100 5599326 Prolonged oral Cannabinoid Administration prevents Neuroinflammation, lowers beta-amyloid Levels and improves Cognitive Performance in Tg APP 2576 Mice. http://www.medworm.com/index.php?rid=5599325&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F8 Conclusions: In summary we have shown that chronically administered cannabinoid showed marked beneficial effects concomitant with inflammation reduction and increased Abeta clearance. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5599325 Mon, 16 Jan 2012 05:00:00 +0100 5599325 Psychological stress in adolescent and adult mice increases neuroinflammation and attenuates the response to LPS challenge http://www.medworm.com/index.php?rid=5599324&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F9 Conclusion: Our results demonstrate that predatory stress, an ethologically relevant stressor, can elicit changes in neuroinflammation and behavior. The predatory stress model may be useful in elucidating mechanisms by which psychological stress modulates diseases with an inflammatory component. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5599324 Mon, 16 Jan 2012 05:00:00 +0100 5599324 Can the benefits of cannabinoid receptor stimulation on neuroinflammation, neurogenesis and memory during normal aging be useful in AD prevention? http://www.medworm.com/index.php?rid=5599323&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F10 Background: Alzheimer's disease has become a growing socio-economical concern in developing countries where increased life expectancy is leading to large aged populations. While curing Alzheimer's disease or stopping its progression does not appear within reach in a foreseeable future, new therapies capable of delaying the pathogenesis would represent major breakthroughs.Presentation of the hypothesisThe growing number of medical benefits of cannabinoids, such as their ability to regulate age-related processes like neuroinflammation, neurogenesis and memory, raise the question of their potential role as a preventive treatment of AD.Testing the hypothesisTo test this hypothesis, epidemiological studies on long term, chronic cannabinoid users could enlighten us on the potential benefits of t... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5599323 Mon, 16 Jan 2012 05:00:00 +0100 5599323 NADPH oxidase and reactive oxygen species contribute to alcohol-induced microglial activation and neurodegeneration http://www.medworm.com/index.php?rid=5584586&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F5 Conclusions: Ethanol activation of microglia and astrocytes, induction of NOX and production of ROS contribute to chronic ethanol-induced neurotoxicity. NOX-ROS and NFkappa-B signaling pathways play important roles in chronic ethanol-induced neuroinflammation and neurodegeneration. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5584586 Thu, 12 Jan 2012 05:00:00 +0100 5584586 Tumor necrosis factor-alpha-mediated threonine 435 phosphorylation of p65 nuclear factor-kappaB subunit in endothelial cells induces vasogenic edema and neutrophil infiltration in the rat piriform cortex following status epilepticus http://www.medworm.com/index.php?rid=5584585&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F6 Conclusion: These findings suggest that impairments of endothelial cell functions via TNF-alpha-mediated p65-Thr 485 NF-kappaB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5584585 Thu, 12 Jan 2012 05:00:00 +0100 5584585 Immunological characterization and transcription profiling of peripheral blood (PB) monocytes in children with autism spectrum disorders (ASD) and specific polysaccharide antibody deficiency (SPAD): Case study. http://www.medworm.com/index.php?rid=5573023&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F4 This study assessed whether these ASD/SPAD children have distinct immunological findings in comparison with ASD/non-SPAD or non-ASD/SPAD children.Case description: We describe 8 ASD/SPAD children with worsening behavioral symptoms/cognitive skills that are triggered by immune insults. These ASD/SPAD children exhibited delayed type food allergy (5/8), treatment-resistant seizure disorders (4/8), and chronic gastrointestinal (GI) symptoms (5/8) at high frequencies. Control subjects included ASD children without SPAD (N=39), normal controls (N=37), and non-ASD children with SPAD (N=12).Discussion and Evaluation: We assessed their innate and adaptive immune responses, by measuring the production of pro-inflammatory and counter-regulatory cytokines by peripheral blood mononuclear cells (PBMCs) ... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5573023 Sat, 07 Jan 2012 05:00:00 +0100 5573023 Endotoxin-induced cytokine and chemokine expression in the HIV-1 transgenic rat http://www.medworm.com/index.php?rid=5561955&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F3 Conclusion: Our data indicate that the continuous presence of HIV-1 viral proteins can have tissue-dependent effects on endotoxin-induced cytokine and chemokine expression in the ET state. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5561955 Wed, 04 Jan 2012 05:00:00 +0100 5561955 Pharmacological inhibition of Akt and downstream pathways modulates the expression of COX-2 and mPGES-1 in activated microglia http://www.medworm.com/index.php?rid=5561956&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F2 Conclusion. Taken together, we demonstrate that blockade of mTOR and/or PI3K/Akt enhances prostanoid production and that PI3K/Akt, GSK-3 and mTOR differently regulate the expression of mPGES-1 and COX-2 in activated primary microglia. Therefore, these pathways are potential targets for the development of novel strategies to modulate neuroinflammation. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5561956 Tue, 03 Jan 2012 05:00:00 +0100 5561956 Innate Immunity in multiple sclerosis white matter lesions: expression of natural cytotoxicity triggering receptor 1 (NCR1) http://www.medworm.com/index.php?rid=5561957&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F9%2F1%2F1 Conclusions: The data presented here show very limited expression of NCR1+ NK cells in MS lesions, the majority of NCR1 expression being accounted for by expression on astrocytes. This is compatible with a role of this cell-type and NCR1 ligand/receptor interactions in the innate immune response in the CNS in MS patients. This is the first report of NCR1 expression on astrocytes in MS tissue: it will now be important to unravel the nature of cellular interactions and signalling mediated through innate receptor expression on astrocytes. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5561957 Mon, 02 Jan 2012 05:00:00 +0100 5561957 Interferon regulatory factor 3 plays an anti-inflammatory role in microglia by activating the PI3K/Akt pathway http://www.medworm.com/index.php?rid=5553269&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F187 Conclusions: Our results show a novel anti-inflammatory role for the PI3K/Akt signaling pathway in microglia. They further suggest that IRF3 gene therapy could facilitate the microglial phenotype switch from proinflammatory ("M1-like") to anti-inflammatory and immunomodulatory ("M2-like"), in part, by augmenting the level of pAkt. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5553269 Fri, 30 Dec 2011 05:00:00 +0100 5553269 Low ficolin-3 levels in early follow-up serum samples are associated with the severity and unfavorable outcome of acute ischemic stroke http://www.medworm.com/index.php?rid=5553271&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F185 Background: A number of data indicate that the lectin pathway of complement activation contributes to the pathophysiology of ischemic stroke. The lectin pathway may be triggered by the binding of mannose-binding lectin (MBL), ficolin-2 or ficolin-3 to different ligands. Although several papers demonstrated the significance of MBL in ischemic stroke, the role of ficolins has not been examined. Methods: Sera were obtained within 12 hours after the onset of ischemic stroke (admission samples) and 3-4 days later (follow-up samples) from 65 patients. The control group comprised 100 healthy individuals and 135 patients with significant carotid stenosis (patient controls). The concentrations of ficolin-2 and ficolin-3, initiator molecules of the lectin complement pathway, were measured by ELISA m... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5553271 Thu, 29 Dec 2011 05:00:00 +0100 5553271 Interleukin-1alpha expression precedes IL-1beta after ischemic brain injury and is localised to areas of focal neuronal loss and penumbral tissues http://www.medworm.com/index.php?rid=5553270&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F186 Conclusions: The early expression of IL-1alpha in areas of focal neuronal injury suggests that it is the major form of IL-1 contributing to inflammation early after cerebral ischemia. This adds to the growing body of evidence that IL-1alpha is a key mediator of the sterile inflammatory response. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5553270 Thu, 29 Dec 2011 05:00:00 +0100 5553270 Complement activating antibodies to myelin oligodendrocyte glycoprotein in neuromyelitis optica and related disorders http://www.medworm.com/index.php?rid=5553272&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F184 Conclusions: We could show for the first time that a subset of AQP4-IgG seronegative patients with NMO and HR-NMO exhibit a MOG-IgG mediated immune response, whereas MOG is not a target antigen in cases with an AQP4-directed humoral immune response. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5553272 Wed, 28 Dec 2011 05:00:00 +0100 5553272 Interleukin-1 beta and neurotrophin-3 synergistically promote neurite growth in vitro http://www.medworm.com/index.php?rid=5545588&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F183 Pro-inflammatory cytokines such as interleukin-1 beta (IL-1beta) are considered to exert detrimental effects during brain trauma and in neurodegenerative disorders. Consistently, it has been demonstrated that IL-1beta suppresses neurotrophin-mediated neuronal cell survival rendering neurons vulnerable to degeneration. Since neurotrophins are also well known to strongly influence axonal plasticity, we investigated here whether IL-1beta has a similar negative impact on neurite growth. We analyzed neurite density and length of organotypic brain and spinal cord slice cultures under the influence of the neurotrophins NGF, BDNF, NT-3 and NT-4. In brain slices, only NT-3 significantly promoted neurite density and length. Surprisingly, a similar increase of neurite growth was induced by IL-1beta. ... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5545588 Mon, 26 Dec 2011 05:00:00 +0100 5545588 Interferon regulatory factor-7 modulates experimental autoimmune encephalomyelitis in mice http://www.medworm.com/index.php?rid=5539242&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F181 Conclusion: Together, our findings suggest that IRF7 signaling is critical for regulation of inflammatory responses in the CNS. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5539242 Fri, 23 Dec 2011 05:00:00 +0100 5539242 Modulation of spinal cord synaptic activity by tumor necrosis factor alpha in a model of peripheral neuropathy http://www.medworm.com/index.php?rid=5526929&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F177 Conclusions: Our results indicate that TNF-alpha may enhance spontaneous transmitter release from primary afferent fibres in the spinal cord DH by modulation of TTX-sensitive sodium channels following sciatic nerve transection. This nerve injury also leads to enhanced sensitivity of presynaptic TRPV1 receptors to endogenous agonist. Modulation of presynaptic receptor activity on primary sensory terminals by TNF-alpha may play an important role in neuropathic pain development. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5526929 Wed, 21 Dec 2011 05:00:00 +0100 5526929 TLR3 signaling is either protective or pathogenic for the development of Theiler's virus-induced demyelinating disease depending on the time of viral infection http://www.medworm.com/index.php?rid=5526928&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F178 Conclusions: These results suggest that TLR3-mediated signaling during viral infection protects against demyelinating disease by reducing the viral load and modulating immune responses. In contrast, premature activation of TLR3 signal transduction prior to viral infection leads to pathogenesis via over-activation of the pathogenic immune response. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5526928 Wed, 21 Dec 2011 05:00:00 +0100 5526928 Insulin-like growth factor-I peptides act centrally to decrease depression-like behavior of mice treated intraperitoneally with lipopolysaccharide http://www.medworm.com/index.php?rid=5526927&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F179 In this study we tested the ability of IGF-I and GPE (the N-terminal tri-peptide derived from IGF-I) to alter depression-like behavior induced by intraperitoneal (i.p.) administration of LPS in a preventive and curative manner. In the first case, IGF-I (1 ug) or GPE (5 ug) was administered i.c.v. to CD-1 mice followed 30 min later by 330 ug/kg body weight i.p. LPS. In the second case, 830 ug/kg body weight LPS was given 24 h prior to either IGF-I or GPE. When administered i.p., LPS induced full-blown sickness assessed as a loss of body weight, decrease in food intake and sickness behavior. None of these indices were affected by IGF-I or GPE. LPS also induced depression-like behavior; assessed as an increased duration of immobility in the tail suspension and forced swim tests. When administ... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5526927 Wed, 21 Dec 2011 05:00:00 +0100 5526927 The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism http://www.medworm.com/index.php?rid=5526926&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F180 Conclusions: Serum neurokinin A levels were elevated in some autistic children and they were significantly correlated to the severity of autism and to serum levels of anti-ribosomal P protein antibodies. However, this is an initial report that warrants further research to determine the pathogenic role of neurokinin A and its possible link to autoimmunity in autism. The therapeutic role of tachykinin receptor antagonists, a potential new class of anti-inflammatory medications, should also be studied in autism. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5526926 Wed, 21 Dec 2011 05:00:00 +0100 5526926 Apolipoprotein E expression is elevated by interleukin 1 and other interleukin 1-induced factors http://www.medworm.com/index.php?rid=5506704&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F175 Conclusion: Conditions of glial activation and hyperexcitation can elevate proinflammatory cytokines, ApoE, glutamate, betaAPP, and its secreted fragments. Because each of these factors promotes glial activation and neuronal hyperexcitation, these relationships have the potential to sustain self-propagating neurodegenerative cycles that could culminate in a progressive neurodegenerative disorder such as Alzheimer's disease. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5506704 Thu, 15 Dec 2011 05:00:00 +0100 5506704 Temporal pattern of expression and colocalization of microglia/macrophage phenotype markers following brain ischemic injury in mice http://www.medworm.com/index.php?rid=5495896&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F174 Conclusions: These data show that the ischemic lesion is accompanied by activation of specific microglia/macrophage phenotype that presents distinctive spatial and temporal features. These different states of microglia/macrophages reflect the complexity of these cells and their ability to differentiate towards a multitude of phenotypes depending on the surrounding micro-environmental signals that can change over time. The data presented in this study provide a basis for understanding this complex response and for developing strategies resulting in promotion of a protective inflammatory phenotype. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5495896 Sat, 10 Dec 2011 05:00:00 +0100 5495896 Increased circulating leukocyte numbers and altered macrophage phenotype correlate with the altered immune response to brain injury in metallothionein (MT) -I/II null mutant mice. http://www.medworm.com/index.php?rid=5488468&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F172 Conclusions: These results contribute to the evidence that MT-I/II-/- mice have altered immune system function and provide a new hypothesis that this alteration is partly responsible for the differences observed in MT-I/II-/- mice after brain injury relative to wild type mice. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5488468 Wed, 07 Dec 2011 05:00:00 +0100 5488468 Adaptive Muller cell responses to microglial activation mediate neuroprotection and coordinate inflammation in the retina http://www.medworm.com/index.php?rid=5488467&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F173 Conclusion: Our findings demonstrate that activated microglia are able to influence Muller cells directly, and initiate a program of bidirectional microglia-Muller cell signaling that can mediate adaptive responses within the retina following injury. In the acute aftermath following initial microglia activation, Muller cell responses may serve to augment initial inflammatory responses across retinal lamina and to guide the intraretinal mobilization of migratory microglia using chemotactic cues and adhesive cell contacts. Understanding adaptive microglia-Muller cell interactions in injury responses can help discover therapeutic cellular targets for intervention in retinal disease. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5488467 Wed, 07 Dec 2011 05:00:00 +0100 5488467 Neuroinflammation in Alzheimer's disease wanes with age http://www.medworm.com/index.php?rid=5477949&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F171 Conclusion: Our data suggest that the association between neuroinflammation and AD is stronger in relatively young patients than in the oldest patients. This age-dependent relationship between inflammation and clinical phenotype of AD has implications for the interpretation of biomarkers and treatment of the disease. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5477949 Wed, 07 Dec 2011 05:00:00 +0100 5477949 CXCR7 antagonism prevents axonal injury during experimental autoimmune encephalomyelitis as revealed by in vivo axial diffusivity http://www.medworm.com/index.php?rid=5477950&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F170 Conclusions: These data suggest that CXCR7 antagonism not only prevents persistent inflammation but also preserves axonal integrity. Thus, targeting CXCR7 modifies both disease severity and recovery during EAE, suggesting a role for this molecule in both phases of disease. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5477950 Tue, 06 Dec 2011 05:00:00 +0100 5477950 Neuropeptide Y inhibits interleukin-1beta-induced phagocytosis by microglial cells http://www.medworm.com/index.php?rid=5470259&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F169 Conclusions: Altogether, we have identified a novel role for NPY in the regulation of microglial phagocytic properties, in an inflammatory context. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5470259 Fri, 02 Dec 2011 05:00:00 +0100 5470259 Lipopolysaccharide-enhanced transcellular transport of HIV-1 across the blood-brain barrier is mediated by luminal microvessel IL-6 and GM-CSF http://www.medworm.com/index.php?rid=5459500&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F167 Elevated levels of cytokines/chemokines contribute to increased neuroinvasion of human immunodeficiency virus type 1 (HIV-1). Previous work showed that lipopolysaccharide (LPS), which is present in the plasma of patients with HIV-1, enhanced transcellular transport of HIV-1 across the blood-brain barrier (BBB) through the activation of p38 mitogen-activated protein kinase (MAPK) signaling in brain microvascular endothelial cells (BMECs). Here, we found that LPS (100 mug/mL, 4 hr) selectively increased interleukin (IL)-6 and granulocyte-macrophage colony-stimulating factor (GM-CSF) release from BMECs. The enhancement of HIV-1 transport induced by luminal LPS was neutralized by treatment with luminal, but not with abluminal antibodies to IL-6 and GM-CSF without affecting paracellular permeab... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5459500 Wed, 30 Nov 2011 05:00:00 +0100 5459500 Neuro-Inflammation, Blood-Brain Barrier, Seizures and Autism http://www.medworm.com/index.php?rid=5459499&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F168 Many children with Autism Spectrum Diseases (ASD) present with seizure activity, but the pathogenesis is not understood. Recent evidence indicates that neuro-inflammation could contribute to seizures. We hypothesize that and mast cell activation due to allergic, environmental and/or stress triggers could lead to focal disruption of the blood-brain barrier and neuro-inflammation, thus contributing to the development of seizures. Treating neuro-inflammation may be useful when anti-seizure medications are ineffective. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5459499 Wed, 30 Nov 2011 05:00:00 +0100 5459499 The acute inflammatory response to intranigral alpha-synuclein differs significantly from intranigral lipopolysaccharide and is exacerbated by peripheral inflammation http://www.medworm.com/index.php?rid=5459501&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F166 Conclusion: These results suggest that the presence of eSNCA protein 'primes' microglia, making them susceptible to environmental proinflammatory challenge. For this reason, we hypothesise that where 'inflammation' contributes to the disease progression in PD, it does so in a punctuate manner (on-off) as a result of systemic events. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5459501 Mon, 28 Nov 2011 05:00:00 +0100 5459501 Differential regional expression patterns of alpha-synuclein, TNF-alpha, and IL-1beta; and variable status of dopaminergic neurotoxicity in mouse brain after Paraquat treatment http://www.medworm.com/index.php?rid=5442959&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F163 Conclusion: The present study demonstrates that PQ induces ROS production and differential alpha-synuclein expression that promotes neuroinflammation in microglia-dependent or -independent manners, and produces different patterns of dopaminergic neurotoxicity in three different regions of mouse brain.Key Words: Paraquat, alpha-synuclein, tyrosine hydroxylase, tumor necrosis factor-alpha, interleukin-1beta, substantia nigra, frontal cortex, hippocampus. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5442959 Thu, 24 Nov 2011 05:00:00 +0100 5442959 Systemic inflammatory challenges compromise survival after experimental stroke via augmenting brain inflammation, blood-brain barrier damage and brain oedema independently of infarct size http://www.medworm.com/index.php?rid=5442958&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F164 Conclusions: Our results suggest that systemic inflammatory conditions induce cerebrovascular inflammation via diverse mechanisms. Increased brain inflammation, blood-brain barrier injury and brain oedema formation can be major contributors to impaired outcome in mice after experimental stroke with systemic inflammatory stimuli, independently of infarct size. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5442958 Thu, 24 Nov 2011 05:00:00 +0100 5442958 Increased interleukin-1beta levels following low dose MDMA induces tolerance against the 5-HT neurotoxicity produced by challenge MDMA. http://www.medworm.com/index.php?rid=5442957&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F165 Conclusions: These results suggest that IL-1beta plays an important role in the development of delayed preconditioning by low dose MDMA. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5442957 Thu, 24 Nov 2011 05:00:00 +0100 5442957 Gliovascular and cytokine interactions modulate brain endothelial barrier in vitro http://www.medworm.com/index.php?rid=5442960&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F162 The glio-vascular unit (G-unit) plays a prominent role in maintaining homeostasis of the blood-brain barrier (BBB) and disturbances in cells forming this unit may seriously dysregulate BBB. The direct and indirect effects of cytokines on cellular components of the BBB are not yet unclear. The present study compares the effects of cytokines and cytokine-treated astrocytes on brain endothelial barrier. 3-dimensional transwell co-cultures of brain endothelium and related-barrier forming cells with astrocytes were used to investigate gliovascular barrier responses to cytokines during pathological stresses. Gliovascular barrier was measured using trans-endothelial electrical resistance (TEER), a sensitive index of in vitro barrier integrity. We found that neither TNF-alpha, IL-1 beta or IFN-gam... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5442960 Wed, 23 Nov 2011 05:00:00 +0100 5442960 Conformational epitopes of myelin oligodendrocyte glycoprotein are targets of potentially pathogenic antibody responses in multiple sclerosis http://www.medworm.com/index.php?rid=5423700&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F161 Conclusions: Thus high-titer reactivity likely represents high-affinity antibodies against pathologically relevant MOG epitopes, that are only present in a small proportion of patients with MS. Our study provides valuable information about requirements of anti-MOG reactivity for being regarded as a prognostic biomarker in a subtype of MS. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5423700 Thu, 17 Nov 2011 05:00:00 +0100 5423700 Peripheral leukocyte counts and outcomes after intracerebral hemorrhage http://www.medworm.com/index.php?rid=5410354&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F160 Conclusions: Greater changes in leukocyte count over the first 72 hours after admission predicted both worse short term and long term functional outcomes after ICH. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5410354 Wed, 16 Nov 2011 05:00:00 +0100 5410354 Neuroimmune modulation following traumatic stress in rats: evidence for an immunoregulatory cascade mediated by c-Src, miRNA222 and PAK1 http://www.medworm.com/index.php?rid=5410355&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F159 Conclusions: Our results suggest that neuroimmune modulation following traumatic stress is mediated by a cascade that involves c-Src-mediated enhancement of miRNA222 expression and downregulation of PAK1, which in turn impairs signaling via IL-1beta/IL1-RI, leading to immunosuppression. The regulatory networks involving c-Src/miRNA222 and PAK1/IL-1RI signaling have significant potential for the development of therapeutic approaches designed to promote recovery following traumatic injury. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5410355 Mon, 14 Nov 2011 05:00:00 +0100 5410355 Reduced inflammation accompanies diminished myelin damage and repair in the NG2 null mouse spinal cord http://www.medworm.com/index.php?rid=5410356&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F158 Conclusions: Loss of NG2 expression leads to decreased proliferation of OPCs, pericytes, and macrophages/microglia, reducing the abundance of all three cell types in demyelinated spinal cord lesions. As a result of these NG2-dependent changes, the course of demyelination and remyelination in NG2 null mice differs from that seen in wild type mice, with both myelin damage and repair being reduced in the NG2 null mouse. These studies identify NG2 as an important factor in regulating myelin processing, suggesting that therapeutic targeting of the proteoglycan might offer a means of manipulating cell behavior in demyelinating diseases. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5410356 Sun, 13 Nov 2011 05:00:00 +0100 5410356 Pro-inflammatory gene expression and neurotoxic effects of activated microglia are attenuated by absence of CCAAT/enhancer binding protein beta http://www.medworm.com/index.php?rid=5401656&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F156 Conclusions: These findings show involvement of C/EBPbeta in the regulation of pro-inflammatory gene expression in glial activation, and demonstrate for the first time a key role for C/EBPbeta in the induction of neurotoxic effects by activated microglia. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5401656 Thu, 10 Nov 2011 05:00:00 +0100 5401656 Microglia use multiple mechanisms to mediate interactions with vitronectin; non-essential roles for the highly-expressed alphav beta3 and alphav beta5integrins http://www.medworm.com/index.php?rid=5401655&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F157 Conclusions: Taken together, this demonstrates that the alphav beta3 and alphav beta5 integrins are not essential for mediating microglial activation responses to vitronectin, but that microglia use multiple redundant receptors to mediate interactions with this ECM protein. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5401655 Thu, 10 Nov 2011 05:00:00 +0100 5401655 Human brain endothelial cells endeavor to immunoregulate CD8 T cells via PD-1 ligand expression in multiple sclerosis. http://www.medworm.com/index.php?rid=5389816&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F155 Conclusions: Our observations suggest that brain endothelial cells contribute to control T cell transmigration into the CNS and immune responses via PD-L2 expression. However, such impact is impaired in MS lesions due to downregulation of endothelium PD-L2 levels. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5389816 Tue, 08 Nov 2011 05:00:00 +0100 5389816 CD200-CD200R dysfunction exacerbates microglial activation and dopaminergic neurodegeneration in a rat model of Parkinson's disease http://www.medworm.com/index.php?rid=5389817&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F154 Conclusions: This study shows that deficits in the CD200-CD200R system exacerbate microglial activation and dopaminergic neurodegeneration in a 6-OHDA-induced rat model of PD. Our results suggest that dysfunction of CD200-CD200R signalling may be involved in the aetiopathogenesis of PD. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5389817 Sun, 06 Nov 2011 04:00:00 +0100 5389817 Effects of betaine on lipopolysaccharide-induced memory impairment in mice and the involvement of GABA transporter 2 http://www.medworm.com/index.php?rid=5389818&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F153 Conclusions: These data suggest that betaine has protective effects against LPS-induced memory impairment and that prevention of LPS-induced changes in GAT2 mRNA expression is crucial to this ameliorating effect. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5389818 Fri, 04 Nov 2011 04:00:00 +0100 5389818 Origin and consequences of brain Toll-like receptor 4 pathway stimulation in an experimental model of depression http://www.medworm.com/index.php?rid=5365322&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F151 Conclusions: Our results suggest that LPS from bacterial translocation is responsible, at least in part, for the TLR-4 activation found in brain after CMS, which leads to release of inflammatory mediators in the CNS. The use of Gram-negative antibiotics offers a potential therapeutic approach for the adjuvant treatment of depression. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5365322 Thu, 03 Nov 2011 04:00:00 +0100 5365322 Poly(ADP-ribose)polymerase-1 modulates microglial responses to amyloid beta http://www.medworm.com/index.php?rid=5365321&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F152 Conclusions: These results identify PARP-1 as a requisite and previously unrecognized factor in Abeta-induced microglial activation, and suggest that the effects of PARP-1 are mediated, at least in part, by its interactions with NF-kappaB. The suppression of Abeta-induced microglial activation and neurotoxicity by PARP-1 inhibition suggests that this approach could be useful in AD and other disorders in which microglial neurotoxicity may contribute. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5365321 Thu, 03 Nov 2011 04:00:00 +0100 5365321 Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis http://www.medworm.com/index.php?rid=5365324&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F149 Conclusion: Taken together, these results demonstrate novel actions of diazoxide as an anti-inflammatory agent, which might contribute to its beneficial effects on EAE through neuroprotection. Treatment with this widely used and well-tolerated drug may be a useful therapeutic intervention in ameliorating MS disease. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5365324 Wed, 02 Nov 2011 04:00:00 +0100 5365324 The contribution of activated astrocytes to Abeta production: Implications for Alzheimer's disease pathogenesis http://www.medworm.com/index.php?rid=5365323&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F150 Conclusions: Cytokines including TNF-alpha+IFN-gamma increase levels of endogenous BACE1, APP, and Abeta and stimulate amyloidogenic APP processing in astrocytes. Oligomeric and fibrillar Abeta42 also increase levels of astrocytic BACE1, APP, and beta-secretase processing. Together, our results suggest a cytokine- and Abeta42-driven feed-forward mechanism that promotes astrocytic Abeta production. Given that astrocytes greatly outnumber neurons, activated astrocytes may represent significant sources of Abeta during neuroinflammation in AD. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5365323 Wed, 02 Nov 2011 04:00:00 +0100 5365323 Lateral Fluid Percussion Injury of the brain induces CCL20 inflammatory chemokine expression in rats http://www.medworm.com/index.php?rid=5365325&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F148 Conclusion: These results demonstrate that the systemic inflammatory reaction to TBI starts earlier than the local brain response and suggest that spleen- and/ or thymus-derived CCL20 might play a role in promoting neuronal injury and central nervous system inflammation in response to mild TBI. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5365325 Mon, 31 Oct 2011 04:00:00 +0100 5365325 Post-traumatic hypoxia exacerbates neurological deficit, neuroinflammation and cerebral metabolism in rats with diffuse traumatic brain injury http://www.medworm.com/index.php?rid=5365326&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F147 Conclusion: Altogether, aggravated behavioural deficits observed in rats with diffuse TAI combined with hypoxia may be induced by enhanced neuroinflammation, and a prolonged period of metabolic dysfunction. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5365326 Fri, 28 Oct 2011 04:00:00 +0100 5365326 Anti-CD20 B-cell depletion enhances monocyte reactivity in neuroimmunological disorders http://www.medworm.com/index.php?rid=5349621&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F146 Conclusions: These data suggest that in neuroimmunological disorders, pro-inflammatory APC activity is controlled by a subset of B-cells which is eliminated concomitantly upon anti-CD20 treatment. While this observation does not conflict with the general concept of B-cell depletion in human autoimmunity, it implies that its safety and effectiveness may further advance by selectively targeting pathogenic B-cell function. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5349621 Wed, 26 Oct 2011 04:00:00 +0100 5349621 HIV-1 and IL-1beta regulate astrocytic CD38 through mitogen-activated protein kinases and nuclear factor-kappaB signaling mechanisms http://www.medworm.com/index.php?rid=5349622&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F145 Background: Infection with human immunodeficiency virus type-1 (HIV)-1 leads to some form of HIV-1-associated neurocognitive disorders (HAND) in approximately half of the cases. The mechanisms by which astrocytes contribute to HIV-1-associated dementia (HAD), the most severe form of HAND, still remain unresolved. HIV-1-encephalitis (HIVE), a pathological correlate of HAD, affects an estimated 9-11% of the HIV-1-infected population. Our laboratory has previously demonstrated that HIVE brain tissues show significant upregulation of CD38, an enzyme involved in calcium signaling, in astrocytes. We also reported an increase in CD38 expression in interleukin (IL)-1beta-activated astrocytes. In the present investigation, we studied regulatory mechanisms of CD38 gene expression in astrocytes activ... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5349622 Tue, 25 Oct 2011 04:00:00 +0100 5349622 Chitotriosidase as a biomarker of cerebral adrenoleukodystrophy http://www.medworm.com/index.php?rid=5338099&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F144 Background: Adrenoleukodystrophy (ALD) is an X-linked peroxisomal disorder characterized by the abnormal beta-oxidation of very long chain fatty acids (VLCFA). In 35-40% of children with ALD, an acute inflammatory process occurs in the central nervous system (CNS) leading to demyelination that is rapidly progressive, debilitating and ultimately fatal. Allogeneic hematopoietic stem cell transplantation (HSCT) can halt disease progression in cerebral ALD (C-ALD) if performed early. In contrast, for advanced patients the risk of morbidity and mortality is increased with transplantation. To date there is no means of quantitating neuroinflammation in C-ALD, nor is there an accepted measure to determine prognosis for more advanced patients. Methods: As cellular infiltration has been observed in ... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5338099 Thu, 20 Oct 2011 04:00:00 +0100 5338099 Differential aquaporin 4 expression during edema build-up and resolution phases of brain inflammation http://www.medworm.com/index.php?rid=5338100&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F143 Conclusions: We conclude that a time lag in AQP4 expression occurs such that the more significant upregulation was achieved only after a delay period. This change in AQP4 expression appears to act as an important determinant in the exacerbation of edema, considering that AQP4 expression is insufficient to counter the water influx during the build-up phase, while the second more pronounced but delayed upregulation is involved in the resolution phase. A better pathophysiological understanding of edema exacerbation, which is observed in many clinical situations, is crucial in pursuing new therapeutic strategies. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5338100 Wed, 19 Oct 2011 04:00:00 +0100 5338100 LPS preconditioning redirects TLR signaling following stroke: TRIF-IRF3 plays a seminal role in mediating tolerance to ischemic injury http://www.medworm.com/index.php?rid=5316835&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F140 Conclusion: Our results characterize several critical mediators of the TLR4 signaling events associated with neuroprotection. LPS preconditioning redirects TLR4 signaling in response to stroke through suppression of NFkappaB activity, enhanced IRF3 activity, and increased anti-inflammatory/type I IFN gene expression. Interestingly, this protective phenotype does not require the suppression of pro-inflammatory mediators. Furthermore, our results highlight a critical role for TRIF-IRF3 signaling as the governing mechanism in the neuroprotective response to stroke. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5316835 Fri, 14 Oct 2011 04:00:00 +0100 5316835 Cautionary notes on the use of NF-kappaB p65 and p50 antibodies for CNS studies http://www.medworm.com/index.php?rid=5316834&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F141 Conclusions: We note that many of the findings in the literature about neuronal NF-kappaB are based on data garnered with antibodies that are not selective for the NF kappaB subunit proteins p65 and p50. The data urge caution in interpreting studies of neuronal NF-kappaB activity in the brain. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5316834 Fri, 14 Oct 2011 04:00:00 +0100 5316834 Brain microvascular pericytes are immunoactive in culture: cytokine, chemokine, nitric oxide, and LRP-1 expression in response to lipopolysaccharide http://www.medworm.com/index.php?rid=5316836&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F139 Conclusions: Our results show that cultured mouse brain microvascular pericytes secrete cytokines, chemokines, and nitric oxide and respond to the innate immune system stimulator LPS. These immune properties of pericytes are likely important in their communication within the neurovascular unit and provide a mechanism by which they participate in neuroinflammatory processes in brain infections and neurodegenerative diseases. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5316836 Thu, 13 Oct 2011 04:00:00 +0100 5316836 Increased levels of HMGB1 and pro-inflammatory cytokines in children with febrile seizures http://www.medworm.com/index.php?rid=5305886&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F135 Conclusions: HMGB1 and pro-inflammatory cytokines were significantly higher in febrile seizure children. Although it is not possible to infer causality from descriptive human studies, our data suggest that HMGB1 and the cytokine network may contribute to the generation of febrile seizures in children. There may be a potential role for anti-inflammatory therapy targeting cytokines and HMGB1 in preventing or limiting febrile seizures or subsequent epileptogenesis in the vulnerable, developing nervous system of children. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5305886 Tue, 11 Oct 2011 04:00:00 +0100 5305886 Toll-like receptor 2 -196 to -174 del polymorphism influences the susceptibility of Han Chinese people to Alzheimer's disease http://www.medworm.com/index.php?rid=5305885&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F136 Conclusions: Our data suggest that the -196 to -174 del/del genotype of TLR2 may increase risk of LOAD in a Northern Han Chinese population. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5305885 Tue, 11 Oct 2011 04:00:00 +0100 5305885 The role of the MYD88-dependent pathway in MPTP-induced brain dopaminergic degeneration http://www.medworm.com/index.php?rid=5305884&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F137 Conclusions. Our results suggest that subacute MPTP-induced dopaminergic degeneration observed in the central nervous system is MyD88-independent, in contrast to our recent observations that this pathway, in the same cohort of animals, is critical in the loss of dopaminergic neurons in the enteric nervous system. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5305884 Tue, 11 Oct 2011 04:00:00 +0100 5305884 Concurrent hippocampal induction of MHC II pathway components and glial activation with advanced aging is not correlated with cognitive impairment http://www.medworm.com/index.php?rid=5305883&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F138 Conclusions: These data demonstrate a novel, coordinated age-related induction of the MHC II immune response pathway and glial activation in the hippocampus, indicating an allostatic shift toward a para-inflammatory phenotype with advancing age. Our findings demonstrate that age-related induction of these aspects of hippocampal neuroinflammation, while a potential contributing factor, is not sufficient by itself to elicit impairment of spatial learning and memory in models of normative aging. Future efforts are needed to understand how neuroinflammation may act synergistically with cognitive-decline specific alterations to cause cognitive impairment. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5305883 Tue, 11 Oct 2011 04:00:00 +0100 5305883 Toll-like receptors in cerebral ischemic inflammatory injury http://www.medworm.com/index.php?rid=5298191&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F134 Cerebral ischemia triggers acute inflammation, which has been associated with an increase in brain damage. The mechanisms that regulate the inflammatory response after cerebral ischemia are multifaceted. An important component of this response is the activation of the innate immune system. However, details of the role of the innate immune system within the complex array of mechanisms in cerebral ischemia remain unclear. There have been recent great strides in our understanding of the innate immune system, particularly in regard to the signaling mechanisms of Toll-like receptors (TLRs), whose primary role is the initial activation of immune cell responses. So far, few studies have examined the role of TLRs in cerebral ischemia. However, work with experimental models of ischemia suggests tha... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5298191 Sat, 08 Oct 2011 04:00:00 +0100 5298191 Inhibitory effect of a tyrosine-fructose Maillard reaction product, 2,4-bis(p-hydroxyphenyl)-2-butenal on amyloid-beta generation and inflammatory reactions via inhibition of NF- kappaB and STAT3 activation in cultured astrocytes and microglial BV-2 cells http://www.medworm.com/index.php?rid=5298193&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F132 Conclusions: These results indicate that 2,4-bis(p-hydroxyphenyl)-2-butenal inhibits neuroinflammatory reactions and amyloidogenesis through inhibition of NF-kappaB and STAT3 activation, and suggest that 2,4-bis(p-hydroxyphenyl)-2-butenal may be useful for the treatment of neuroinflammatory diseases like Alzheimer's disease. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5298193 Fri, 07 Oct 2011 04:00:00 +0100 5298193 Comparing the immunosuppressive potency of naive marrow stromal cells and Notch-transfected marrow stromal cells http://www.medworm.com/index.php?rid=5298192&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F133 Conclusion: The results demonstrated that the immunosuppressive activity of the expanded NICD-transfected MSCs is comparable to the parental MSCs, in spite of the appearance of a small number of senescent-like cells. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5298192 Fri, 07 Oct 2011 04:00:00 +0100 5298192 In vivo imaging of lymphocytes in the CNS reveals different behaviour of naive T cells in health and autoimmunity http://www.medworm.com/index.php?rid=5298194&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F131 Conclusions: The activation status rather than antigen specificity or regulatory phenotype is the central requirement for CD4+ T cell migration within healthy CNS tissue. However, under inflammatory conditions naive CD4+ T cells can get access to CNS parenchyma and partially migrate along inflammation-induced extracellular SHG structures, which are similar to those seen in lymphoid organs. These SHG structures apparently provide essential migratory signals for naive CD4+ T cells within the diseased CNS. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5298194 Thu, 06 Oct 2011 04:00:00 +0100 5298194 Generation of reactive oxygen species in 1-methyl-4-phenylpyridinium (MPP+) treated dopaminergic neurons occurs as an NADPH oxidase-dependent two-wave cascade http://www.medworm.com/index.php?rid=5287397&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F129 Conclusions: A two-wave cascade of ROS production is active in nigral dopaminergic neurons in response to neurotoxicity-induced superoxide. Our findings allow us to conclude that superoxide generated by NADPH oxidase present in nigral neurons contributes to the loss of such neurons in PD. Losartan suppression of nigral-cell superoxide production suggests that angiotensin receptor blockers have potential as PD preventatives. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5287397 Wed, 05 Oct 2011 04:00:00 +0100 5287397 Delayed inflammatory mRNA and protein expression after spinal cord injury http://www.medworm.com/index.php?rid=5287396&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F130 Conclusions: These data demonstrate that inflammation-related genes are chronically up-regulated after SCI and may contribute to further tissue loss. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5287396 Wed, 05 Oct 2011 04:00:00 +0100 5287396 Serum Lipid Profiles are Associated with Disability and MRI Outcomes in Multiple Sclerosis http://www.medworm.com/index.php?rid=5287399&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F127 Conclusions: Serum lipid profile has modest effects on disease progression in MS. Worsening disability is associated with higher levels of LDL, total cholesterol and triglycerides. Higher HDL is associated with lower levels of acute inflammatory activity. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5287399 Tue, 04 Oct 2011 04:00:00 +0100 5287399 Lipopolysaccharide modulates astrocytic S100B secretion: a study in cerebrospinal fluid and astrocyte cultures from rats http://www.medworm.com/index.php?rid=5287398&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F128 Conclusions: Together, these data contribute to the understanding of the effects of LPS on astrocytes, particularly on S100B secretion, and help us to interpret cerebrospinal fluid and serum changes for this protein in neuroinflammatory diseases. Moreover, non-brain S100B-expressing tissues may be differentially regulated, since LPS administration did not lead to increased serum levels of S100B. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5287398 Tue, 04 Oct 2011 04:00:00 +0100 5287398 Up-regulation of dorsal root ganglia BDNF and trkB receptor in inflammatory pain: an in vivo and in vitro study http://www.medworm.com/index.php?rid=5275563&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F126 Conclusions: Based on our current experimental results, we conclude that inflammation and TNF-alpha up-regulate the BDNF-trkB system in DRG. This phenomenon suggests that up-regulation of BDNF in DRG may, in addition to its post-synaptic effect in spinal dorsal horn, act as an autocrine and/or paracrine signal to activate the pre-synaptic trkB receptor and regulate synaptic excitability in pain transmission, thereby contributing to the development of hyperalgesia. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5275563 Fri, 30 Sep 2011 04:00:00 +0100 5275563 Curcumin is a potent modulator of microglial gene expression and migration http://www.medworm.com/index.php?rid=5262523&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F125 Conclusions: Collectively, our results suggest that curcumin is a potent modulator of the microglial transcriptome. Curcumin attenuates microglial migration and triggers a phenotype with anti-inflammatory and neuroprotective properties. Thus, curcumin could be a nutraceutical compound to develop immuno-modulatory and neuroprotective therapies for the treatment of various neurodegenerative disorders. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5262523 Thu, 29 Sep 2011 04:00:00 +0100 5262523 Strain-dependent variation in the early transcriptional response to CNS injury using a cortical explant system http://www.medworm.com/index.php?rid=5262526&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F122 Conclusions: The short-term cortical explant model employed in this study provides a basic approach to evaluate an early transcriptional response to neurological damage, and can identify expression differences in genes that are influenced by genetic background. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5262526 Mon, 26 Sep 2011 04:00:00 +0100 5262526 Reactive oxygen species drive herpes simplex virus (HSV)-1-induced proinflammatory cytokine production by murine microglia http://www.medworm.com/index.php?rid=5262525&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F123 Conclusions: Data presented herein demonstrate that HSV infection induces proinflammatory responses in microglia through NADPH oxidase-dependent ROS and the activation of MAPKs. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5262525 Mon, 26 Sep 2011 04:00:00 +0100 5262525 Lipocalin 2 in the central nervous system host response to systemic lipopolysaccharide administration http://www.medworm.com/index.php?rid=5262524&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F124 Conclusions: 1) Lcn2 production is strongly induced in the CNS by systemic LPS injection, 2) in addition to Lcn2 production at key gateways of bacterial entry to the CNS, neurons may be a target for the actions of Lcn2, which is apparently taken up by these cells, and 3) the cellular functions of Lcn2 in the CNS remain enigmatic. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5262524 Mon, 26 Sep 2011 04:00:00 +0100 5262524 Pro-inflammatory cytokines and lipopolysaccharide induce changes in cell morphology, and upregulation of ERK1/2, iNOS and sPLA2-IIA expression in astrocytes and microglia http://www.medworm.com/index.php?rid=5252058&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F121 Conclusion: These results demonstrated the utility of BV-2 and HAPI cells as models for investigation on cytokine and LPS induction of iNOS, and DITNC astrocytes for induction of sPLA2-IIA. In addition, results further demonstrated that cytokine-induced sPLA2-IIA is attributed mainly to astrocytes and not microglial cells. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5252058 Sat, 24 Sep 2011 04:00:00 +0100 5252058 Activation of retinal microglia rather than microglial cell density correlates with retinal neovascularization in the mouse model of oxygen-induced retinopathy http://www.medworm.com/index.php?rid=5252059&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F120 Conclusion: Density of microglial cells does not correlate with vascular obliteration or revascularization. But the time course of the activation of microglia indicates that they may be involved in retinal neovascularization during the hypoxic phase. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5252059 Fri, 23 Sep 2011 04:00:00 +0100 5252059 Overexpression of serine racemase in retina and overproduction of D-serine in eyes of streptozotocin-induced diabetic retinopathy http://www.medworm.com/index.php?rid=5252060&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F119 Conclusions: Increased expression of SR in retina and higher levels of glutamate and D-serine in aqueous humor of STZ-treated rats may result from activation of the JNK pathway in diabetic sequelae. Our data suggest that the inflammatory conditions that prevail during DR result in elevation of D-serine, a neurotransmitter contributing to glutamate toxicity, potentially exacerbating the death of retinal ganglion cells in this condition. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5252060 Thu, 22 Sep 2011 04:00:00 +0100 5252060 Treatment with gelsolin reduces brain inflammation and apoptotic signaling in mice following thermal injury http://www.medworm.com/index.php?rid=5239891&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F118 Background: Burn survivors develop long-term cognitive impairment with increased inflammation and apoptosis in the brain. Gelsolin, an actin-binding protein with capping and severing activities, plays a crucial role in the septic response. We investigated if gelsolin infusion could attenuate neural damage in burned mice. Methods: Mice with 15% total body surface area burns were injected intravenously with bovine serum albumin as placebo (2 mg/kg), or with low (2 mg/kg) or high doses (20 mg/kg) of gelsolin. Samples were harvested at 8, 24, 48 and 72 hours postburn. The immune function of splenic T cells was analyzed. Cerebral pathology was examined by hematoxylin/eosin staining, while activated glial cells and infiltrating leukocytes were detected by immunohistochemistry. Cerebral cytokine ... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5239891 Wed, 21 Sep 2011 04:00:00 +0100 5239891 Cerebral Amyloid Angiopathy-related Inflammation Presenting with Steroid-responsive Higher Brain Dysfunction: Case Report and Review of the Literature http://www.medworm.com/index.php?rid=5228038&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F116 A 56-year-old man noticed discomfort in his left lower limb, followed by convulsion and numbness in the same area. Magnetic resonance imaging (MRI) showed white matter lesions in the right parietal lobe accompanied by leptomeningeal or leptomeningeal and cortical post-contrast enhancement along the parietal sulci. The patient also exhibited higher brain dysfunction corresponding with the lesions on MRI. Histological pathology disclosed beta-amyloid in the blood vessels and perivascular inflammation, which highlights the diagnosis of cerebral amyloid angiopathy (CAA)-related inflammation. Pulse steroid therapy was so effective that clinical and radiological findings immediately improved.CAA-related inflammation is a rare disease, defined by the deposition of amyloid proteins within the lept... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5228038 Wed, 14 Sep 2011 04:00:00 +0100 5228038 Sinomenine inhibits microglial activation by A-beta and confers neuroprotection http://www.medworm.com/index.php?rid=5228037&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F117 Conclusions: Sinomenine prevents oligomeric A-beta-induced microglial activation, and confers protection against indirect neurotoxicity to hippocampal cells. These results raise the possibility that sinomenine may have therapeutic potential for the treatment of Alzheimer's diseases as well as other diseases that involve neuroinflammation. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5228037 Wed, 14 Sep 2011 04:00:00 +0100 5228037 Nogo receptor is involved in the adhesion of dendritic cells to myelin http://www.medworm.com/index.php?rid=5211063&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F113 Conclusions: These results indicate that a lack of NgR1/2 expression promotes the adhesion of DCs to myelin. This interaction could be important in neuroinflammatory disorders such as multiple sclerosis in which peripheral immune cells come into contact with myelin debris. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5211063 Fri, 09 Sep 2011 04:00:00 +0100 5211063 Vascular endothelial growth factor-A (VEGF-A) and chemokine ligand (CCL2) genes are upregulated in peripheral blood mononuclear cells (PBMCs) in Indian amyotrophic lateral sclerosis (ALS) patients http://www.medworm.com/index.php?rid=5211062&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F114 Conclusion VEGF-A and CCL2 mRNA upregulation in PBMCs may have a clinico-pathological/etiological/epidemiological association with ALS pathogenesis. The cross-cultural and cross-ethnic investigations of these molecules could determine if they have any role in enhancing the mean survival time unique to Indian ALS patients. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5211062 Fri, 09 Sep 2011 04:00:00 +0100 5211062 Activation of matrix metalloproteinases following anti-Abeta immunotherapy; implications for microhemorrhage occurrence. http://www.medworm.com/index.php?rid=5211061&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F115 Conclusions: Since the MMP2 and MMP9 systems are heavily implicated in the pathophysiology of intracerbral hemorrhage, these data may provide a potential mechanism of microhemorrhage due to immunotherapy. Increased activity of the MMP system, therefore, is likely to be a major factor in increased microhemorrhage occurrence. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5211061 Fri, 09 Sep 2011 04:00:00 +0100 5211061 Osteoarthritis accelerates and exacerbates Alzheimer's disease pathology in mice http://www.medworm.com/index.php?rid=5211064&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F112 Conclusion: This work supports a model by which peripheral inflammation triggers the development of neuroinflammation and subsequently the induction of AD pathology. Better understanding of the link between peripheral localized inflammation, whether in the form of osteoarthritis, atherosclerosis or other conditions, and brain inflammation, may prove critical to our understanding of the pathophysiology of disorders such as Alzheimer's, Parkinson's and other neurodegenerative diseases. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5211064 Wed, 07 Sep 2011 04:00:00 +0100 5211064 Low plasma progranulin levels in children with autism http://www.medworm.com/index.php?rid=5197550&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F111 Conclusions: Plasma progranulin levels were reduced in a subgroup of patients with autism. Progranulin insufficiency in some patients with autism may result in many years of reduced neutrotrophic support together with cumulative damage in association with dysregulated inflammation that may have a role in autism. However, these data should be treated with caution until further investigations are performed, with a larger subject population, to determine whether the decrease of plasma progranulin levels is a mere consequence of autism or has a pathogenic role in the disease. The role of progranulin therapy should also be studied in autism. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5197550 Sun, 04 Sep 2011 23:00:00 +0100 5197550 Wallerian degeneration: the innate-immune response to traumatic nerve injury http://www.medworm.com/index.php?rid=5176471&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F109 Traumatic injury to peripheral nerves results in the loss of neural functions. Recovery by regeneration depends on the cellular and molecular events of Wallerian degeneration that injury induces distal to the lesion site, the domain through which severed axons regenerate back to their target tissues. Innate-immunity is central to Wallerian degeneration since innate-immune cells, functions and molecules that are produced by immune and non-immune cells are involved. The innate-immune response helps to turn the peripheral nerve tissue into an environment that supports regeneration by removing inhibitory myelin and by upregulating neurotrophic properties. The characteristics of an efficient innate-immune response are rapid onset and conclusion, and the orchestrated interplay between Schwann ce... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5176471 Mon, 29 Aug 2011 23:00:00 +0100 5176471 Wallerian degeneration: Gaining perspective on inflammatory events after peripheral nerve injury http://www.medworm.com/index.php?rid=5176470&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F110 In this review, we first provide a brief historical perspective, discussing how peripheral nerve injury (PNI) may have caused World War I. We then consider the initiation, progression, and resolution of the cellular inflammatory response after PNI, before comparing the PNI inflammatory response with that induced by spinal cord injury (SCI).In contrast with central nervous system (CNS) axons, those in the periphery have the remarkable ability to regenerate after injury. Nevertheless, peripheral nervous system (PNS) axon regrowth is hampered by nerve gaps created by injury. In addition, the growth-supportive milieu of PNS axons is not sustained over time, precluding long-distance regeneration. Therefore, studying PNI could be instructive for both improving PNS regeneration and recovery after... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5176470 Mon, 29 Aug 2011 23:00:00 +0100 5176470 The role of tumor necrosis factor-alpha and TNF-alpha receptors in cerebral arteries following cerebral ischemia in rat http://www.medworm.com/index.php?rid=5171252&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F107 Conclusion: The present study shows that cerebral ischemia and organ culture induce expression of TNF-alpha and its receptors in the walls of cerebral arteries and that upregulation is transcriptionally regulated via the MEK/ERK pathway. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5171252 Sat, 27 Aug 2011 23:00:00 +0100 5171252 Brain pericytes among cells constituting the blood-brain barrier are highly sensitive to tumor necrosis factor-alpha, releasing matrix metalloproteinase-9 and migrating in vitro http://www.medworm.com/index.php?rid=5164368&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F106 Conclusion: These findings suggest that pericytes are most sensitive to TNF-alpha in terms of MMP-9 release, and are the major source of MMP-9 at the BBB. This pericyte-derived MMP-9 initiated cellular migration of pericytes, which might be involved in pericyte loss in the damaged BBB. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5164368 Thu, 25 Aug 2011 23:00:00 +0100 5164368 Air pollution and the brain: Subchronic diesel exhaust exposure causes neuroinflammation and elevates early markers of neurodegenerative disease http://www.medworm.com/index.php?rid=5164369&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F105 Conclusions: Together, the data support that the midbrain may be more sensitive to the neuroinflammatory effects of subchronic air pollution exposure. However, the DE-induced elevation of proteins associated with neurodegenerative diseases was limited to only the higher exposures, suggesting that air pollution-induced neuroinflammation may precede preclinical markers of neurodegenerative disease in the midbrain. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5164369 Tue, 23 Aug 2011 23:00:00 +0100 5164369 Cigarette smoke extract upregulates heme oxygenase-1 via PKC/NADPH oxidase/ROS/PDGFR/PI3K/Akt pathway in mouse brain endothelial cells http://www.medworm.com/index.php?rid=5147635&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F104 Conclusions: Taken together, these results suggested that PPCSE-induced HO-1 expression is mediated by a PC-PLC/PKCdelta/NADPH oxidase-dependent PDGFR/PI3K/Akt pathway in bEnd.3 cells. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5147635 Tue, 23 Aug 2011 23:00:00 +0100 5147635 Reduction of Neutrophil Activity Decreases Early Microvascular Injury after Subarachnoid Haemorrhage. http://www.medworm.com/index.php?rid=5147636&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F103 ConclusionsOur results implicate neutrophils in early microvascular injury after SAH and indicate that treatments which reduce neutrophil activity can be beneficial in limiting microvascular injury after SAH. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5147636 Thu, 18 Aug 2011 23:00:00 +0100 5147636 Anandamide inhibits Theiler's virus induced VCAM-1 in brain endothelial cells and reduces leukocyte transmigration in a model of blood brain barrier by activation of CB1 receptors http://www.medworm.com/index.php?rid=5147637&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F102 Conclusions: Our results suggest that CB1 receptor dependent VCAM-1 inhibition is a novel mechanism for AEA-reduced leukocyte transmigration and contribute to a better understanding of the mechanisms underlying the beneficial role of endocannabinoid system in the Theiler's virus model of MS. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5147637 Wed, 17 Aug 2011 23:00:00 +0100 5147637 Peripheral anti-inflammatory effects explain the ginsenosides paradox between poor brain distribution and anti-depression efficacy http://www.medworm.com/index.php?rid=5133661&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F100 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5133661 Mon, 15 Aug 2011 23:00:00 +0100 5133661 Increased neuroinflammatory and arachidonic acid cascade markers, and reduced synaptic proteins, in brain of HIV-1 transgenic rats http://www.medworm.com/index.php?rid=5133660&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F101 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5133660 Mon, 15 Aug 2011 23:00:00 +0100 5133660 A role for DNA-dependent activator of interferon regulatory factor in the recognition of herpes simplex virus type 1 by glial cells http://www.medworm.com/index.php?rid=5121116&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F99 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5121116 Thu, 11 Aug 2011 23:00:00 +0100 5121116 CRP gene variation affects early development of Alzheimer's disease-related plaques http://www.medworm.com/index.php?rid=5121119&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F96 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5121119 Wed, 10 Aug 2011 23:00:00 +0100 5121119 Correction: Vascular endothelial growth factor-A (VEGF-A) and chemokine ligand-2 (CCL2) in amyotrophic lateral sclerosis (ALS) patients http://www.medworm.com/index.php?rid=5121118&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F97 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5121118 Wed, 10 Aug 2011 23:00:00 +0100 5121118 Methylsalicylate 2-O-beta-D-lactoside, a novel salicylic acid analogue, acts as an anti-inflammatory agent on microglia and astrocytes http://www.medworm.com/index.php?rid=5121117&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F98 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5121117 Wed, 10 Aug 2011 23:00:00 +0100 5121117 Severe depression is associated with increased microglial quinolinic acid in subregions of the anterior cingulate gyrus: Evidence for an immune-modulated glutamatergic neurotransmission? http://www.medworm.com/index.php?rid=5111325&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F94 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5111325 Tue, 09 Aug 2011 23:00:00 +0100 5111325 Aspirin-triggered lipoxin A4 attenuates LPS-induced pro-inflammatory responses by inhibiting activation of NF-kappaB and MAPKs in BV-2 microglial cells http://www.medworm.com/index.php?rid=5111324&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F95 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5111324 Tue, 09 Aug 2011 23:00:00 +0100 5111324 TLR4 mutation reduces microglial activation, increases Abeta deposits and exacerbates cognitive deficits in a mouse model of Alzheimer's disease http://www.medworm.com/index.php?rid=5111327&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F92 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5111327 Mon, 08 Aug 2011 23:00:00 +0100 5111327 ELISA measurement of specific non-antigen-bound antibodies to Abeta1-42 monomer and soluble oligomers in sera from Alzheimer's disease, mild cognitively impaired, and noncognitively impaired subjects http://www.medworm.com/index.php?rid=5111326&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F93 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5111326 Mon, 08 Aug 2011 23:00:00 +0100 5111326 The PPAR-gamma agonist pioglitazone modulates inflammation and induces neuroprotection in parkinsonian monkeys http://www.medworm.com/index.php?rid=5099100&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F91 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5099100 Thu, 04 Aug 2011 23:00:00 +0100 5099100 Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria. http://www.medworm.com/index.php?rid=5099101&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F90 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5099101 Wed, 03 Aug 2011 23:00:00 +0100 5099101 Poly(I:C) promotes TNFalpha/TNFR1-dependent oligodendrocyte death in mixed glial cultures http://www.medworm.com/index.php?rid=5089646&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F89 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5089646 Tue, 02 Aug 2011 23:00:00 +0100 5089646 A role for tumor necrosis factor-alpha in ischemia and ischemic preconditioning http://www.medworm.com/index.php?rid=5089648&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F87 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5089648 Mon, 01 Aug 2011 23:00:00 +0100 5089648 HIV-1 Tat activates indoleamine 2,3 dioxygenase in murine organotypic hippocampal slice cultures in a p38 mitogen-activated protein kinase-dependent manner http://www.medworm.com/index.php?rid=5089647&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F88 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5089647 Mon, 01 Aug 2011 23:00:00 +0100 5089647 Heteroarylketones inhibit astroglial interleukin-6 expression via a STAT3/NF-kappaB signaling pathway http://www.medworm.com/index.php?rid=5071883&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F86 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5071883 Thu, 28 Jul 2011 23:00:00 +0100 5071883 Myelin-phagocytosing macrophages modulate autoreactive T cell proliferation http://www.medworm.com/index.php?rid=5064869&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F85 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5064869 Sun, 24 Jul 2011 23:00:00 +0100 5064869 Transcriptional analysis of rat piriform cortex following exposure to the organophosphonate anticholinesterase sarin and induction of seizures http://www.medworm.com/index.php?rid=5054165&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F83 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5054165 Wed, 20 Jul 2011 23:00:00 +0100 5054165 Transcriptional responses of the nerve agent-sensitive brain regions amygdala, hippocampus, piriform cortex, septum, and thalamus following exposure to the organophosphonate anticholinesterase sarin http://www.medworm.com/index.php?rid=5054164&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F84 ${item.shortDescription} (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5054164 Wed, 20 Jul 2011 23:00:00 +0100 5054164 Estrogens regulate neuroinflammatory genes via estrogen receptors alpha and beta in the frontal cortex of middle-aged female rats http://www.medworm.com/index.php?rid=5041673&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F82 Conclusions: These findings provide evidence that E2, 16alpha-LE2 and DPN modulate the expression of neuroinflammatory genes in the frontal cortex of middle-aged female rats via both ERalpha and ERbeta. We propose that ERbeta is a promising target to suppress regulatory functions of glial cells in the E2-deprived female brain and in various neuroinflammatory diseases. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5041673 Tue, 19 Jul 2011 23:00:00 +0100 5041673 Neuroinflammation induces glial aromatase expression in the uninjured songbird brain http://www.medworm.com/index.php?rid=5041674&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F81 Conclusions: These studies are among the first to examine a neuroinflammatory response in the songbird brain following mechanical brain injury and to describe a novel neuroimmune signal to initiate aromatase expression in glia. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5041674 Sun, 17 Jul 2011 23:00:00 +0100 5041674 Increased local concentration of complement C5a contributes to incisional pain in mice http://www.medworm.com/index.php?rid=5011091&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F80 Conclusions: This study demonstrates that high locally generated C5a levels are present in wounds for at least 72 hours after incision. In skin, C5a contributes to hypersensitivity after incision, but increased responsiveness of cutaneous nociceptors to C5a was not evident in incised skin. Thus, high local concentrations of C5a produced in wounds likely contribute to postoperative pain. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5011091 Wed, 06 Jul 2011 23:00:00 +0100 5011091 S-Nitrosoglutathione reduces oxidative injury and promotes mechanisms of neurorepair following traumatic brain injury in rats http://www.medworm.com/index.php?rid=5001089&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F78 Conclusion: Our findings indicate the participation of peroxynitrite in the pathobiology of TBI. GSNO treatment of TBI not only reduces peroxynitrite but also protects the integrity of the neurovascular unit, indicating that GSNO blunts the deleterious effects of peroxynitrite. A long-term treatment of TBI with the same low dose of GSNO promotes synaptic plasticity and enhances the expression of neurotrophic factors. These results support that GSNO reduces the levels of oxidative metabolites, protects the neurovascular unit, and promotes neurorepair mechanisms in TBI. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5001089 Tue, 05 Jul 2011 23:00:00 +0100 5001089 Fingolimod modulates microglial activation to augment markers of remyelination http://www.medworm.com/index.php?rid=5001091&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F76 Conclusions: The results presented indicate that modulation of S1P receptors can ameliorate pathological effectors associated with microglial activation leading to a subsequent increase in protein and morphological markers of remyelination. In addition, sphingosine-1-phosphate receptor 5 is implicated in promoting remyelination in vitro. This knowledge may be of benefit for treatment of chronic microglial inflammation in multiple sclerosis. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5001091 Mon, 04 Jul 2011 23:00:00 +0100 5001091 CCL2 / MCP-1 modulation of microglial activation and proliferation http://www.medworm.com/index.php?rid=5001090&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F77 Conclusion: These data indicate that, while causing migration and proliferation of microglia, MCP-1 does not appear to directly activate an inflammatory response in this cell type, and therefore, other factors may be necessary to cause the changes that result in the neuronal damage commonly observed in situations where MCP-1 levels are elevated. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=5001090 Mon, 04 Jul 2011 23:00:00 +0100 5001090 Lack of macrophage migration inhibitory factor in mice does not affect hallmarks of the inflammatory/immune response during the first week after stroke http://www.medworm.com/index.php?rid=4978651&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F75 Conclusions: We conclude that MIF does not affect major components of the inflammatory/immune response during the first week after experimental stroke. Based on present and previous evidence, we propose that the deleterious MIF-mediated effects in stroke depend primarily on an intraneuronal and/or interneuronal action. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4978651 Tue, 28 Jun 2011 23:00:00 +0100 4978651 Granulocyte colony stimulating factor attenuates inflammation in a mouse model of amyotrophic lateral sclerosis http://www.medworm.com/index.php?rid=4978652&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F74 Conclusions: GCSF attenuated inflammation in the CNS and the periphery in a mouse model of ALS and thereby delayed the progression of the disease. This mechanism of action targeting inflammation provides a new perspective of the usage of GCSF in the treatment of ALS. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4978652 Mon, 27 Jun 2011 23:00:00 +0100 4978652 Lymph node-derived donor encephalitogenic CD4+ T cells in C57BL/6 mice adoptive transfer experimental autoimmune encephalomyelitis highly express GM-CSF and T-bet http://www.medworm.com/index.php?rid=4962586&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F73 Experimental autoimmune encephalomyelitis (EAE) is a relevant animal model for the human demyelinating inflammatory disorder of the central nervous system (CNS), multiple sclerosis (MS). Induction of EAE by adoptive transfer allows studying the role of the donor T lymphocyte in disease pathogenesis. It has been challenging to reliably induce adoptive transfer EAE in C57BL/6 (H-2b) mice. The goal of this study was to develop a reproducible and high yield protocol for adoptive transfer EAE in C57BL/6 mice. A step-wise experimental approach permitted us to develop a protocol that resulted in a consistent relatively high disease incidence of ~70% in recipient mice. Donor mice were immunized with myelin oligodendrocyte glycoprotein (MOG)p35-55 in complete Freund's adjuvant (CFA) followed by per... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4962586 Thu, 23 Jun 2011 23:00:00 +0100 4962586 Prevention of the beta-amyloid peptide-induced inflammatory process by inhibition of double-stranded RNA-dependent protein kinase in primary murine mixed co-cultures http://www.medworm.com/index.php?rid=4962587&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F72 Conclusion: In spite of the complexity of the innate immune response, PKR inhibition could be an interesting anti-inflammatory strategy in AD. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4962587 Wed, 22 Jun 2011 23:00:00 +0100 4962587 Temporal and sequential changes of glial cells and cytokine expression during neuronal degeneration after transient global ischemia in rats http://www.medworm.com/index.php?rid=4955860&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F70 Conclusion: Ischemic stress in 4VO, activated glial cells in areas beyond CA1 in the lag phase. Pyramidal neurons were injured in CA1 from the end of the lag phase and then neurons reduced in CA1 in the exponential phase. After neuron death began, the influence of dead cells on glial cells and cytokine expression gradually became stronger than the influence by ischemic stress. Therefore, from the deceleration phase, changes in glial cells and cytokine production were likely caused by dead cells. Cytokine interaction in the microenvironment may determine the functions of IL-1, IL-1, IL-4, IL-6 and IFN-in all four phases. The function of GM-CSF and TNF- in the deceleration phase may be neurotrophic.. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4955860 Tue, 21 Jun 2011 23:00:00 +0100 4955860 A lack of association between hyperserotonemia and the increased frequency of serum anti-myelin basic protein auto-antibodies in autistic children http://www.medworm.com/index.php?rid=4955859&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F71 Background: One of the most consistent biological findings in autism is the elevated blood serotonin levels. Immune abnormalities, including autoimmunity with production of brain specific auto-antibodies, are also commonly observed in this disorder. Hyperserotonemia may be one of the contributing factors to autoimmunity in some patients with autism through the reduction of T-helper (Th) 1-type cytokines. We are the first to investigate the possible role of hyperserotonemia in the induction of autoimmunity, as indicated by serum anti-myelin-basic protein (anti-MBP) auto-antibodies, in autism. Methods: Serum levels of serotonin and anti-MBP auto-antibodies were measured, by ELISA, in 50 autistic patients, aged between 5 and 12 years, and 30 healthy-matched children. Results: Autistic childre... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4955859 Tue, 21 Jun 2011 23:00:00 +0100 4955859 Melittin restores proteasome function in an animal model of ALS http://www.medworm.com/index.php?rid=4947376&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F69 Amyotrophic lateral sclerosis (ALS) is a paralyzing disorder characterized by the progressive degeneration and death of motor neurons and occurs both as a sporadic and familial disease. Mutant SOD1 (mtSOD1) in motor neurons induces vulnerability to the disease through protein misfolding, mitochondrial dysfunction, oxidative damage, cytoskeletal abnormalities, defective axonal transport- and growth factor signaling, excitotoxicity, and neuro-inflammation.Melittin is a 26 amino acid protein and is one of the components of bee venom which is used in traditional Chinese medicine to inhibit of cancer cell proliferation and is known to have anti-inflammatory and anti-arthritic effects.The purpose of the present study was to determine if melittin could suppress motor neuron loss and protein misfo... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4947376 Sun, 19 Jun 2011 23:00:00 +0100 4947376 Midazolam suppresses interleukin-1beta-induced interleukin-6 release from rat glial cells http://www.medworm.com/index.php?rid=4939707&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F68 Conclusion: These results strongly suggest that midazolam inhibits IL-1beta-induced IL-6 release in rat C6 glioma cells via suppression of STAT3 activation. Midazolam may affect immune system function in the CNS. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4939707 Thu, 16 Jun 2011 23:00:00 +0100 4939707 Increased cerebral (R)-[11C]PK11195 uptake and glutamate release in a rat model of traumatic brain injury: a longitudinal pilot study http://www.medworm.com/index.php?rid=4939708&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F67 Background: The aim of the present study was to investigate microglia activation over time following traumatic brain injury (TBI) and to relate these findings to glutamate release.Procedures: Sequential dynamic (R)-[11C]PK11195 PET scans were performed in rats 24 hours before (baseline), and one and ten days after TBI using controlled cortical impact, or a sham procedure. Extracellular fluid (ECF) glutamate concentrations were measured using cerebral microdialysis. Brains were processed for histopathology and (immuno)-histochemistry. Results: Ten days after TBI, (R)-[11C]PK11195 binding was significantly increased in TBI rats compared with both baseline values and sham controls (p (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4939708 Mon, 13 Jun 2011 23:00:00 +0100 4939708 Exogenous nitric oxide decreases brain vascular inflammation, leakage and venular resistance during Plasmodium berghei ANKA infection in mice http://www.medworm.com/index.php?rid=4905807&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F66 Conclusions: These results indicate that the protective effect of exogenous NO on murine CM is associated with decreased brain vascular expression of inflammatory markers resulting in attenuated endothelial junction damage and facilitating blood flow. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4905807 Mon, 06 Jun 2011 23:00:00 +0100 4905807 Loss of function mutations in the progranulin gene are related to pro-inflammatory cytokine dysregulation in frontotemporal lobar degeneration patients http://www.medworm.com/index.php?rid=4905808&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F65 In this study, we analyzed serum levels of the pro-inflammatory mediators IL-6, TNF-alpha and IL-18 in FTLD patients with or without PGRN mutations, at both pre-symptomatic and symptomatic stages. We provide evidence that circulating IL-6 is increased in PGRN-mutated FTLD patients, as compared to both PGRN non-mutated FTLD patients and controls. In contrast, levels of IL-6 were not altered in asymptomatic subjects carrying the PGRN mutations. Finally, TNF-alpha and IL-18 serum levels did not differ among all groups of included subjects.We conclude that the profile of circulating pro-inflammatory cytokines is altered in PGRN-related symptomatic FTLD. Thus, our findings point to IL-6 as a possible specific mediator and a potential therapeutic target in this monogenic disease, suggesting that... Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4905808 Sun, 05 Jun 2011 23:00:00 +0100 4905808 Increased expression of cystine/glutamate antiporter in multiple sclerosis http://www.medworm.com/index.php?rid=4896732&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F63 Conclusions: Together, these results reveal that increased expression of the cystine/glutamate antiporter system xc- in MS provides a link between inflammation and excitotoxicity in demyelinating diseases. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4896732 Thu, 02 Jun 2011 23:00:00 +0100 4896732 Momordica charantia (bitter melon) attenuates high-fat diet-associated oxidative stress and neuroinflammation http://www.medworm.com/index.php?rid=4896731&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F64 Conclusions: Functional foods such as BM offer a unique therapeutic strategy to improve obesity-associated peripheral inflammation and neuroinflammation. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4896731 Thu, 02 Jun 2011 23:00:00 +0100 4896731 P2X7 receptor activation ameliorates CA3 neuronal damage via a tumor necrosis factor-alpha-mediated pathway in the rat hippocampus following status epilepticus http://www.medworm.com/index.php?rid=4886898&cid=s_32242_25_f&fid=32242&url=http%3A%2F%2Fwww.jneuroinflammation.com%2Fcontent%2F8%2F1%2F62 Conclusions: These findings suggest that TNF-alpha induction by P2X7 receptor activation may ameliorate SE-induced CA3 neuronal damage via enhancing NF-kappaB p65-Ser276 and p65-Ser311 phosphorylations. (Source: Journal of Neuroinflammation) Journal of Neuroinflammation journals http://www.medworm.com/rss/comments.php?id=4886898 Wed, 01 Jun 2011 23:00:00 +0100 4886898