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Expression of complement system components during aging and amyloid deposition in APP transgenic miceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: Early but not late components of the mouse complement system show an age-dependent increase in expression. The response to amyloid deposition is comparatively smaller. The low expression of C3 and C5 and failure to upregulate C5 and downstream components differs from human AD brain and likely contributes to the lack of full complement activation in APP transgenic mice. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - November 17, 2009 Category: Neurology Authors: Julia ReichwaldSimone DannerKarl-Heinz WiederholdMatthias Staufenbiel Source Type: journals

The C5a anaphylatoxin receptor CD88 is expressed in presynaptic terminals of hippocampal mossy fibresEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: These results demonstrate that CD88 is expressed on presynaptic terminals of mossy fibres within the CA3 region of the hippocampus. Although the role of CD88 on mossy fibres remains to be established, their involvement in synaptic/cellular plasticity, and in cognitive disorders such as Alzheimer's disease deserves investigation. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - November 16, 2009 Category: Neurology Authors: James CraneGilang BaiquniRobert SullivanJohn LeePanakj SahStephen TaylorPeter NoakesTrent Woodruff Source Type: journals

Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: Together these findings suggest that Annexin A1 null mice have an impaired capacity to develop EAE. Furthermore strategies aiming at reducing Annexin A1 functions or expression in T cells might represent a novel therapeutic approach for multiple sclerosis. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - November 13, 2009 Category: Neurology Authors: Nikolaos PaschalidisAsif IqbalFrancesco MaioneElisabeth WoodMauro PerrettiRod FlowerFulvio D'Acquisto Source Type: journals

Administration of S-nitrosoglutathione after traumatic brain injury protects the neurovascular unit and reduces secondary injury in a rat model of controlled cortical impactEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: GSNO is a promising candidate to be evaluated in humans after brain trauma because it not only protects the traumatic penumbra from secondary injury and improves overall tissue structure but also maintains the integrity of BBB and reduces neurologic deficits following CCI in a rat model of experimental TBI. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - November 4, 2009 Category: Neurology Authors: Mushfiquddin KhanYeong-Bin ImAnadakumar ShunmugavelAnne GilgRamanpreet DhindsaAvtar SinghInderjit Singh Source Type: journals

Cerebellar Purkinje cells incorporate immunoglobulins and immunotoxins in vitro: implications for human neurological disease and immunotherapeuticsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: Purkinje cells in rat organotypic cultures incorporate and clear host (rat) and non-host (human or donkey) IgG or IgM, independent of the immunoglobulin's reactivity with Purkinje cell antigens. This property permits real-time study of immunoglobulin-Purkinje cell interaction using fluorochrome IgG conjugates, and can allow Purkinje cell-specific delivery of IgG-conjugated pharmacological agents. Antibodies to intracellular Purkinje cell proteins could potentially be incorporated intracellularly to produce cell injury. Antibodies used therapeutically, including immunotoxins, may also be taken up and cause Purk...
Source: Journal of Neuroinflammation - October 29, 2009 Category: Neurology Authors: Kenneth HillSusan ClawsonJohn RoseNoel CarlsonJohn Greenlee Source Type: journals

Estrogen treatment following severe burn injury reduces brain inflammation and apoptotic signalingEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, 149 adult Sprague-Dawley male rats received 3rd degree 40% total body surface area (TBSA) burns. Fifteen minutes following burn injury, the animals received a subcutaneous injection of either placebo (n=72) or 17 beta-estradiol (n=72). Brains were harvested at 0.5, 1, 2, 4, 6, 8, 12, 18, and 24 hours after injury from the control (n=5), placebo (n=8/time point), and estrogen treated animals (n=8/time point). The brain cytokine levels were measured using the ELISA method. In addition, we assessed the levels of phosphorylated-ERK, phosphorylated-Akt, active caspase-3, and the levels of cleaved PARP at the 24 h...
Source: Journal of Neuroinflammation - October 21, 2009 Category: Neurology Authors: Joshua GatsonDavid MaassJames SimpkinsAhamed IdrisJoseph MineiJane Wigginton Source Type: journals

Central nesfatin-1 expressing neurons are sensitive to peripheral inflammatory stimulusEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Recently, a novel factor with anorexigenic properties was identified and called nesfatin-1. This protein (82 aac) is not only expressed in peripheral organs but it is also found in neurons located in specific structures including the hypothalamus and the brainstem, two sites strongly involved in food intake regulation. Here, we studied whether some of the neurons that become activated following an injection of an anorectic dose of lipopolysaccharides (LPS) exhibit a nesfatin-1 phenotype. To this end, we used double immunohistochemistry to target the expression of the immediate-early gene c-fos and of nesfatin-1 on coronal ...
Source: Journal of Neuroinflammation - September 23, 2009 Category: Neurology Authors: Marion BonnetEmilie PecchiJerome TrouslardAndre JeanMichel DallaportaJean-Denis Troadec Source Type: journals

Resveratrol inhibits prostaglandin formation in IL-1beta-stimulated SK-N-SH neuronal cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Resveratrol, a polyphenol present in grapes and red wine, has been studied due to its vast pharmacological activity. It has been demonstrated that resveratrol inhibits production of inflammatory mediators in different in vitro and in vivo models. Our group recently demonstrated that resveratrol reduced the production of prostaglandin (PG) E2 and 8-isoprostane in rat activated microglia. In a microglial-neuronal coculture, resveratrol reduced neuronal death induced by activated microglia. However, less is known about its direct roles in neurons. In the present study, we investigated the effects of resveratrol on interleukin...
Source: Journal of Neuroinflammation - September 13, 2009 Category: Neurology Authors: Lena WendeburgAntonio Carlos Pinheiro de OliveiraHarsharan BhatiaEduardo Candelario-JalilBernd Fiebich Source Type: journals

Possible role of glial cells in the onset and progression of Lyme neuroborreliosisEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: Our results support the notion that innate responses of glia to B. burgdorferi initiate/mediate the inflammation seen in acute LNB, and show that neuronal apoptosis occurs in this context. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - August 24, 2009 Category: Neurology Authors: Geeta RameshJuan BordaAmy GillErin RibkaLisa MoriciPeter MottramDale MartinMary JacobsPeter DidierMario Philipp Source Type: journals

Expression of P2 nucleotide receptors varies with age and sex in murine brain microgliaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Microglia are implicated in multiple neurodegenerative disorders, many of which display sexual dimorphisms and have symptom onsets at different ages. P2 purinergic receptors are critical for regulating various microglial functions, but little is known about how their expression varies with age or sex. Therefore, comprehensive information about purinergic receptor expression in normal microglia, in both sexes, over age is necessary if we are to better understand their roles in the healthy and diseased CNS. We analyzed the expression of all fourteen rodent P2X and P2Y receptors in CD11b+ cells freshly-isolated from the brain...
Source: Journal of Neuroinflammation - August 24, 2009 Category: Neurology Authors: Jessica CrainMaria NikodemovaJyoti Watters Source Type: journals

Replication by the Epistasis Project of the interaction between the genes for IL-6 and IL-10 in the risk of Alzheimer's diseaseEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: We suggest that dysregulation of both IL-6 and IL-10 in some elderly people, due in part to genetic variations in the two genes, contributes to the development of AD. Thus, inflammation facilitates the onset of sporadic AD. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - August 22, 2009 Category: Neurology Authors: Onofre CombarrosCornelia van DuijnNaomi HammondOlivia BelbinAlejandro Arias-VasquezMario Cortina-BorjaMichael LehmannYurii AulchenkoMaaike SchuurHeike KolschReinhard HeunGordon WilcockKristelle BrownPatrick KehoeRachel HarrisonEliecer CotoVictoria Alvarez Source Type: journals

Reduction of lipoxidative load by secretory phospholipase A2 inhibition protects against neurovascular injury following experimental stroke in ratEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: sPLA2-derived oxidative products contribute to significant neurovascular damage, and treatment with sPLA2 inhibitor DEDA ameliorates secondary injury by reducing exacerbations from lipoxidative stress. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - August 12, 2009 Category: Neurology Authors: Nasrul HodaAnandakumar ShunmugavelInderjit SinghAvtar SinghMushfiquddin Khan Source Type: journals

Beyond blood brain barrier breakdown - in vivo detection of occult neuroinflammatory foci by magnetic nanoparticles in high field MRIEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: VSOP showed a higher sensitivity in detecting BBB alterations compared to Gd-DTPA enhanced MRI, providing complementary information of macrophage/microglia activity in inflammatory plaques that has not been visualized by conventional means. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - August 5, 2009 Category: Neurology Authors: Eva TysiakPatrick AsbachOrhan AktasHelmar WaicziesMaureen SmythJoerg SchnorrMatthias TaupitzJens Wuerfel Source Type: journals

NNZ-2566 treatment inhibits neuroinflammation and pro-inflammatory cytokine expression induced by experimental penetrating ballistic-Like brain injury in ratsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: Collectively, these results suggest that the neuroprotective effects of NNZ-2566 may, in part, be functionally attributed to the compound's ability to modulate expression of multiple neuroinflammatory mediators in the injured brain. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - August 4, 2009 Category: Neurology Authors: Hans WeiXi-Chun LuDeborah ShearAnu WaghrayChangping YaoFrank TortellaJitendra Dave Source Type: journals

Cellular immune response to intrastriatally implanted allogeneic bone marrow stromal cells in a rat model of Parkinson's diseaseEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: MSC, when implanted into the striatum of allogeneic animals, provoke a marked immune response which is not sufficient to clear these cells by 22-24 days post-transplantation. In the experimental paradigm in this study, MSC did not prevent nigrostriatal dopamine depletion and its associated behavioral deficits. Additional studies are indicated to clarify the effects of this immune response on MSC survival and function before initiating trials with these cells in patients with PD or other neurodegenerative disorders. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - June 5, 2009 Category: Neurology Authors: Dianne CampDavid LoefflerDiane FarrahJade BornemanPeter LeWitt Source Type: journals

Unique aspects of transcriptional regulation in neurons - nuances in NFkappaB and Sp1-related factorsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The unique physiology and function of neurons create differences in their cellular physiology, including their regulation of gene expression. We began several years ago exploring the relationships between the NFkappaB transcription factor, neuronal survival, and glutamate receptor activation in telencephalic neurons. These studies led us to conclude that this population of cells is nearly incapable of activating the NFkappaB that is nonetheless expressed at reasonable levels. A subset of the kappaB cis elements are instead bound by members of the Sp1 family in neurons. Also surprising was our discovery that Sp1 itself, typ...
Source: Journal of Neuroinflammation - May 18, 2009 Category: Neurology Authors: Xianrong R. Mao, Andrea M. Moerman-Herzog, Yuzhi Chen and Steven W. Barger Source Type: journals

Neuroinflammation and MMPs: potential therapeutic targets in neonatal hypoxic-ischemic injuryEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Exposure to hypoxic-ischemic insults during the neonatal or perinatal developmental periods produces various forms of pathology. Injuries that occur in response to these events often manifest as severe cognitive and/or motor disturbances over time. Due to difficulties regarding the early diagnosis and treatment of hypoxic-ischemic injury, there is a growing need for effective therapies that can be delivered at delayed time points. Much of the research into mechanisms of neural injury has focused on molecular targets associated with excitotoxicity and free oxygen radicals. Despite repeated success in animal models, these co...
Source: Journal of Neuroinflammation - April 15, 2009 Category: Neurology Authors: Christopher C Leonardo and Keith R Pennypacker Source Type: journals

Cellular localization of kinin B1 receptor in the spinal cord of streptozotocin-diabetic rats with a fluorescent [Nα-Bodipy]-des-Arg9-bradykininEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: The induction and up-regulation of B1R in glial and sensory cells of the spinal cord in STZ-diabetic rats reinforce the idea that kinin B1R is an important target for drug development in pain processes. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - March 26, 2009 Category: Neurology Authors: Sébastien Talbot, Patrick Théberge-Turmel, Dalinda Liazoghli, Jacques Sénécal, Pierrette Gaudreau and Réjean Couture Source Type: journals

Cellular localization of kinin B1 receptor in the spinal cord of streptozotocin-diabetic rats with a fluorescent agonist, [Nalpha-Bodipy]-des-Arg9-bradykininEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: The induction and up-regulation of B1R in glial and sensory cells of the spinal cord in STZ-diabetic rats reinforce the idea that kinin B1R is an important target for drug development in pain processes. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - March 26, 2009 Category: Neurology Authors: Sebastien Talbot, Patrick Theberge-Turmel, Dalinda Liazoghli, Jacques Senecal, Pierrette Gaudreau and Rejean Couture Source Type: journals

Modulation of inducible nitric oxide synthase expression by sumoylationEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions Our results demonstrate that SUMOylation regulates NOS2 expression in astrocytes, and point to modification of C/EBPb as a possible mechanism of action. Targeting the SUMOylation pathway may therefore offer a novel means to regulate inflammatory NOS2 expression in neurological conditions and diseases. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - March 26, 2009 Category: Neurology Authors: Candan A Akar and Douglas L Feinstein Source Type: journals

Acetaminophen inhibits neuronal inflammation and protects neurons from oxidative stressEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The objectives of this study are to determine the effects of acetaminophen on cultured brain neurons survival and inflammatory factor expression when exposed to oxidative stress. Methods: Cerebral cortical cultured neurons are pretreated with acetaminophen and then exposed to the superoxide-generating compound menadione (5 uM). Cell survival is assessed by MTT assay and inflammatory protein (of tumor necrosis factor alpha, interleukin-1, macrophage inflammatory protein alpha, and RANTES) release quantitated by ELISA. Expression of pro- and anti-apoptotic proteins is assessed by western blots. Results: Acetaminophen has pro...
Source: Journal of Neuroinflammation - March 16, 2009 Category: Neurology Authors: Debjani Tripathy and Paula Grammas Source Type: journals

Lipopolysaccharide-induced interleukin-6 production is controlled by glycogen synthase kinase-3 and STAT3 in the brainEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: STAT3 and GSK3 cooperatively promote neuroinflammation, providing novel targets for anti-inflammatory intervention. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - March 11, 2009 Category: Neurology Authors: Eleonore Beurel and Richard S. Jope Source Type: journals

A MT1-MMP/NF-kappaB signalling axis as a checkpoint controller of COX-2 expression in CD133(+) U87 glioblastoma cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: We provide evidence for enhanced COX-2 expression in CD133(+) glioma cells, and direct cell-based evidence of NF-kappaB-mediated COX-2 regulation by MT1-MMP. The biological significance of such checkpoint control may account for COX-2-dependent mechanisms of inflammatory balance responsible of therapy resistance phenotype of cancer stem cells. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - March 9, 2009 Category: Neurology Authors: Borhane Annabi, Carl Laflamme, Asmaa Sina, Marie-Paule Lachambre and Richard Beliveau Source Type: journals

Influence of HFE variants and cellular iron on monocyte chemoattractant protein-1Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: Our results demonstrate that HFE polymorphisms influence the synthesis and release of MCP-1. The mechanism of action involves cellular iron status but it appears there could be additional influences such as ER stress. Finally, these data demonstrate a pharmacogenetic effect of HFE polymorphisms on the ability of minocycline to inhibit MCP-1 secretion. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - February 19, 2009 Category: Neurology Authors: Ryan M Mitchell, Sang Y Lee, William T Randazzo, Zachary Simmons and James R Connor Source Type: journals

Antiphospholipid antibodies: Paradigm in transitionEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: The current paradigm of aPL holds that they are important in thrombosis, but they may have much wider clinical significance, possibly of special interest in neurology. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - January 20, 2009 Category: Neurology Authors: Lawrence L Horstman, Wenche Jy, Carlos J Bidot, Yeon S Ahn, Roger E Kelley, Robert Zivadinov, Amir H. Maghzi, Masoud Etemadifar, Seyed Ali Mousavi and Alireza Minagar Source Type: journals

Absence of the complement regulatory molecule CD59a leads to exacerbated neuropathology after traumatic brain injury in miceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: These data emphasize an important role of CD59 in mediating protection from secondary neuronal cell death and further underscore the key role of the terminal complement pathway in the pathophysiology of traumatic brain injury. The exact mechanisms of complement MAC-induced secondary neuronal cell death after head injury require further investigation. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - January 8, 2009 Category: Neurology Authors: Philip F Stahel, Michael A Flierl, B Paul Morgan, Ivonne Persigehl, Christiane Stoll, Claudia Conrad, Basel M Touban, Wade R Smith, Kathryn Beauchamp, Oliver I Schmidt, Wolfgang Ertel and Iris Leinhase Source Type: journals

Astrocytes play a key role in activation of microglia by persistent Borna disease virus infectionEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Neonatal Borna disease virus (BDV) infection of the rat brain is associated with microglial activation and damage to certain neuronal populations. Since persistent BDV infection of neurons is nonlytic in vitro, activated microglia have been suggested to be responsible for neuronal cell death in vivo. However, the mechanisms of activation of microglia in neonatally BDV-infected rat brains remain unclear. Our previous studies have shown that activation of microglia by BDV in culture requires the presence of astrocytes as neither the virus nor BDV-infected neurons alone activate microglia. Here, we evaluated the mechanisms wh...
Source: Journal of Neuroinflammation - November 11, 2008 Category: Neurology Authors: Mikhail V Ovanesov, Yavuz Ayhan, Candie Wolbert, Krisztina Moldovan, Christian Sauder and Mikhail V Pletnikov Source Type: journals

Inflammaging as a prodrome to Alzheimer's diseaseEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Recently, the term "inflammaging" was coined by Franceshci and colleagues to characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly the from traditional five cardinal features of acute inflammation in that it is characterized by a relative decline in adaptive immunity and T-helper 2 responses and is associated with increased innate immunity by cells of the mononuclear phagocyte lineage. While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individua...
Source: Journal of Neuroinflammation - November 11, 2008 Category: Neurology Authors: Brian Giunta, Francisco Fernandez, William V Nikolic, Demian Obregon, Elona Rrapo, Terrence Town and Jun Tan Source Type: journals

TNF signaling inhibition in the CNS: implications for normal brain function and neurodegenerative diseaseEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The role of tumor necrosis factor (TNF) as an immune mediator has long been appreciated but its function in the brain is still unclear. TNF receptor 1 (TNFR1) is expressed in most cell types, and can be activated by binding of either soluble TNF (solTNF) or transmembrane TNF (tmTNF), with a preference for solTNF; whereas TNFR2 is expressed primarily by microglia and endothelial cells and is preferentially activated by tmTNF. Elevation of solTNF is a hallmark of acute and chronic neuroinflammation as well as a number of neurodegenerative conditions including ischemic stroke, Alzheimer's (AD), Parkinson's (PD), amyotrophic l...
Source: Journal of Neuroinflammation - October 17, 2008 Category: Neurology Authors: Melissa K McCoy and Malú G Tansey Source Type: journals

Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosisEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: The results indicate that atypical extra- and intracellular pleomorphic and cystic forms of Borrelia burgdorferi and local neuroinflammation occur in the brain in chronic Lyme neuroborreliosis. The persistence of these more resistant spirochete forms, and their intracellular location in neurons and glial cells, may explain the long latent stage and persistence of Borrelia infection. The results also suggest that Borrelia burgdorferi may induce cellular dysfunction and apoptosis. The detection and recognition of atypical, cystic and granular forms in infected tissues is essential for the diagnosis and the treatm...
Source: Journal of Neuroinflammation - September 25, 2008 Category: Neurology Authors: Judith Miklossy, Sandor Kasas, Anne D Zurn, Sherman McCall, Sheng Yu and Patrick L McGeer Source Type: journals

Corticosteroids reverse cytokine-induced block of survival and differentiation of oligodendrocyte progenitor cells from ratsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: Our results show that treatment of oligodendrocyte precursors with the inflammatory cytokines TNF-alpha and IFN-gamma block the differentiation of oligodendrocyte precursors at the level of the differentiation of the voltage-gated ion currents. Co-treatment with corticosteroids at the time of cytokine application restores to a considerable extent survival and differentiation of oligodendrocytes at the level of morphological, myelin protein as well as ion current maturation suggesting the option for a functional restoration of cytokine-damaged immature oligodendrocytes. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - September 22, 2008 Category: Neurology Authors: Stefan A Mann, Beatrix Versmold, Romy Marx, Sabine Stahlhofen, Irmgard D Dietzel, Rolf Heumann and Richard Berger Source Type: journals

Sepsis causes neuroinflammation and concomitant decrease of cerebral metabolismEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: Together, the present study highlights the complexity of sepsis induced early impairment of neuronal metabolism and activity. Since our model uses techniques that determine parameters relevant to the clinical setting, it might be a useful tool to develop brain specific therapeutic strategies for human septic encephalopathy. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - September 15, 2008 Category: Neurology Authors: Alexander Semmler, Sven Hermann, Florian Mormann, Marc Weberpals, Stephan A Paxian, Thorsten Okulla, Michael Schafers, Markus P Kummer, Thomas Klockgether and Michael T Heneka Source Type: journals

Transient middle cerebral artery occlusion induces microglial priming in the lumbar spinal cord: a novel model of neuroinflammationEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: The advantages to this method are that it yields a reproducible cortical lesion, the extent of which is predictable using behavioural testing during the period of ischemia, with upper motor neuron involvement and downstream priming, but not full activation, of microglia in the lumbar spinal cord. In addition, survival is excellent following the 30 minutes of occlusion, rendering this a novel and useful model for examining the effects of microglial priming in the spinal motor neuron pool. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - July 7, 2008 Category: Neurology Authors: Katie Moisse, Ian Welch, Tracy Hill, Kathryn Volkening and Michael J Strong Source Type: journals

Acute hemorrhagic demyelination in a murine model of multiple sclerosisEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
This study demonstrates the development of hemorrhagic demyelination in TMEV infected C57BL/6 mice within 24 hours of inducing this condition through intravenous administration of CD8 T cell restricted peptide. This study is also the first demonstration of rapid demyelination in a TMEV resistant non-demyelinating strain without transgenic alterations or pharmacologically induced immunosuppression. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - July 7, 2008 Category: Neurology Authors: Istvan Pirko, Georgette L Suidan, Moses Rodriguez and Aaron J Johnson Source Type: journals

Characterization of early and terminal complement proteins associated with polymorphonuclear leukocytes in vitro and in vivo after spinal cord injuryEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: Data presented here provide the first characterization of early and terminal complement proteins associated with PMNs in vitro and in vivo after SCI. Data also suggest a role for PMNs in the local internalization or deliverance of complement and complement activation in the post-SCI environment. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - June 25, 2008 Category: Neurology Authors: Hal X Nguyen, Manuel D Galvan and Aileen J Anderson Source Type: journals

GRK5 deficiency exaggerates inflammatory changes in TgAPPsw miceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: The results demonstrate that GRK5 deficiency in vivo significantly exaggerates microgliosis and astrogliosis in the presence of an inflammatory initiator, such as the excess fibrillar A-beta and the subsequent active inflammatory reactions in the TgAPPsw mice. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - June 3, 2008 Category: Neurology Authors: Longxuan Li, Jun Liu and William Z Suo Source Type: journals

Squamosamide derivative FLZ protects dopaminergic neurons against inflammation-mediated neurodegeneration through the inhibition of NADPH oxidase activityEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: Taken together, our results clearly demonstrate that FLZ is effective in protecting against LPS- and MPTP-induced neurotoxicity, and the mechanism of this protection appears to be due, at least in part, to inhibition of PHOX activity and to prevention of microglial activation. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - May 28, 2008 Category: Neurology Authors: Dan Zhang, Xiaoming Hu, Sung-Jen Wei, Jie Liu, Huiming Gao, Li Qian, Belinda Wilson, Gengtao Liu and Jau-Shyong Hong Source Type: journals

VEGF receptor antagonist Cyclo-VEGI reduces inflammatory reactivity and vascular leakiness and is neuroprotective against acute excitotoxic striatal insultEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: An antagonist for VEGF receptor-mediated signaling, Cyclo-VEGI, has shown efficacy in a broad spectrum of activity against striatal excitotoxic insult including inhibition of microgliosis, reduction in leakiness of BBB and parenchymal infiltration of plasma fibrinogen and in conferring significant protection for striatal neurons. Antagonism of VEGF-mediated activity, possibly targeting VEGF receptors on reactive microglia, is suggested as a neuroprotective mechanism against inflammatory reactivity and a novel strategy to attenuate acute excitotoxic damage. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - May 20, 2008 Category: Neurology Authors: Jae K Ryu and James G McLarnon Source Type: journals

Neuroinflammatory response to lipopolysaccharide is exacerbated in mice genetically deficient in cyclooxygenase-2Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: These results show that inhibiting COX-2 activity can exacerbate the inflammatory response to LPS, possibly by increasing glial cells activation and upregulating the STAT3 and SOCS3 pathways in the brain. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - May 19, 2008 Category: Neurology Authors: Saba Aid, Robert Langenbach and Francesca Bosetti Source Type: journals

Plaque complement activation and cognitive loss in Alzheimer's diseaseEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: Both early-stage (iC3b) and late-stage (C9) complement activation occurs on neocortical plaques in subjects across the cognitive spectrum; contrary to previous reports, C9 is present on some diffuse plaques. Because of high correlations between complement-stained and Bielschowsky-stained plaque counts, quantitative assessment of the extent to which complement activation may mediate the relationship between plaques and cognitive function could not be performed. Additional studies with animal models of AD (if late-stage complement activation can be demonstrated), or possibly a trial in AD patients with an inhibi...
Source: Journal of Neuroinflammation - March 11, 2008 Category: Neurology Authors: David A Loeffler, Dianne M Camp and David A Bennett Source Type: journals

Neuroinflammation mediated by IL-1 beta increases susceptibility of dopamine neurons to degeneration in an animal model of Parkinson's diseaseEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: These data provide insight into the etiology of PD and support a role for inflammation as a risk factor for the development of neurodegenerative disease. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - February 27, 2008 Category: Neurology Authors: James B Koprich, Casper Reske-Nielsen, Prabhakar Mithal and Ole Isacson Source Type: journals

The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspectiveEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Elevation of the proinflammatory cytokine Interleukin-1 (IL-1) is an integral part of the local tissue reaction to central nervous system (CNS) insult. The discovery of increased IL-1 levels in patients following acute injury and in chronic neurodegenerative disease laid the foundation for two decades of research that has provided important details regarding IL-1's biology and function in the CNS. IL-1 elevation is now recognized as a critical component of the brain's patterned response to insults, termed neuroinflammation, and of leukocyte recruitment to the CNS. These processes are believed to underlie IL-1's function in...
Source: Journal of Neuroinflammation - February 26, 2008 Category: Neurology Authors: Solomon S Shaftel, W. Sue T Griffin and M. Kerry O'Banion Source Type: journals

Complement anaphylatoxin C5a neuroprotects through regulation of glutamate receptor subunit 2 in vitro and in vivoEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: Complement C5a neuroprotects through regulation of GluR2 receptor subunit. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - January 29, 2008 Category: Neurology Authors: Piali Mukherjee, Sunil Thomas and Giulio MARIA Pasinetti Source Type: journals

Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/AktEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: We demonstrate that pioglitazone protects dopaminergic neurons against LPS insult at least via inhibiting iNOS expression and NO generation, which is potentially mediated via inhibition of p38 MAPK activity. In addition, the PI3K pathway actively participates in the negative regulation of LPS-induced NO production. Our findings suggest that PPAR-gamma activation may involve differential regulation of p38 MAPK and of the PI3K/Akt pathway in the regulation of the inflammatory process. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - January 18, 2008 Category: Neurology Authors: Bin Xing, Tao Xin, Randy LEE Hunter and Guoying Bing Source Type: journals

Perispinal etanercept: Potential as an Alzheimer therapeuticEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Tumor necrosis factor-alpha (TNF) is one of a number of systemic and immunomodulating cytokines that generally act to promote acute-phase reactions but can drive degenerative changes when chronically elevated. Traditional focus on TNF has been directed at these inflammation-related functions. Of particular relevance to intersections between neuroinflammation and neurodegeneration is the ability of TNF to increase expression of interleukin-1 (IL-1), which in turn increases production of the precursors necessary for formation of amyloid plaques, neurofibrillary tangles, and Lewy bodies. More recent data have revealed that TN...
Source: Journal of Neuroinflammation - January 10, 2008 Category: Neurology Authors: W. Sue T. Griffin Source Type: journals

Rapid cognitive improvement in Alzheimer's disease following perispinal etanercept administrationEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
This report details rapid cognitive improvement, beginning within minutes, using this same anti-TNF treatment modality, in a patient with late-onset Alzheimer's disease. Rapid cognitive improvement following perispinal etanercept may be related to amelioration of the effects of excess TNF-alpha on synaptic mechanisms in Alzheimer's disease and provides a promising area for additional investigation and therapeutic intervention. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - January 9, 2008 Category: Neurology Authors: Edward L. Tobinick and Hyman Gross Source Type: journals

Does gamma-aminobutyric acid (GABA) influence the development of chronic inflammation in rheumatoid arthritis?Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Background: Recent studies have demonstrated a role for spinal p38 MAP kinase (MAPK) in the development of chronic inflammation and peripheral arthritis and a role for GABA in the inhibition of p38 MAPK mediated effects. Integrating these data suggests that GABA may play a role in downregulating mechanisms that lead to the production of proinflammatory agents such as interleukin-1, interleukin-6, and matrix metalloproteinase 3, agents implicated in the pathogenesis of rheumatoid arthritis (RA). Genetic studies have also associated RA with members of the p38 MAPK pathway. We propose a hypothesis for an inefficient GABA sign...
Source: Journal of Neuroinflammation - January 3, 2008 Category: Neurology Authors: James M Kelley, Laura B Hughes and S. LOUIS Bridges Source Type: journals

Osteopetrotic (op/op) mice have reduced microglia, no Abeta deposition, and no changes in dopaminergic neuronsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusion: In contrast to a prior report we did not detect AI^2 deposition in the central nervous system of op/op mice at 30 days, 60 days or 7 months of age and there was a normal number of dopaminergic neurons. This indicates that op/op mice may be useful to examine the effects of microglia on neurodegenerative disease progression by breeding them to different transgenic mouse models. In addition, the lack of CSF-1 does not appear to affect CD200 expression by neurons but we did note a decrease in the substantia nigra of op/op and WT mice, suggesting that this may be a mechanism by which microglia control may be attenua...
Source: Journal of Neuroinflammation - December 20, 2007 Category: Neurology Authors: Yoichi Kondo, Cynthia A Lemere and Timothy J Seabrook Source Type: journals

Differential effects of Th1, monocyte/macrophage and Th2 cytokine mixtures on early gene expression for glial and neural-related molecules in central nervous system mixed glial cell cultures: neurotrophins, growth factors and structural proteinsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: Each of the three cytokine mixtures induced specific changes in gene expression that could be altered by pharmacologic strategies to promote protection of the central nervous system. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - December 18, 2007 Category: Neurology Authors: Robert P Lisak, Joyce A Benjamins, Beverly Bealmear, Liljana Nedelkoska, Bin Yao, Susan Land and Diane Studzinski Source Type: journals

Amyloid precursor protein modulates beta-catenin degradationEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Conclusions: We have provided strong evidence that APP modulates beta-catenin degradation in vitro and in vivo. Future studies may investigate whether APP processing is necessary for beta-catenin degradation, and determine if excessive APP expression contributes to AD pathogenesis through abnormal beta-catenin downregulation. (Source: Journal of Neuroinflammation)
Source: Journal of Neuroinflammation - December 10, 2007 Category: Neurology Authors: Yuzhi Chen and Angela M Bodles Source Type: journals