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- W2155172987 abstract "Alzheimer's disease (AD) is an age-related dementia, characterized by amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss in the brain. Components of the complement system, known to produce a local inflammatory reaction, are associated with the plaques and tangles in AD brain, and thus a role for complement-mediated inflammation in the acceleration or progression of disease has been proposed. A complement activation product, C5a, is known to recruit and activate microglia and astrocytes in vitro by activation of a G protein-coupled cell-surface C5aR. Here, oral delivery of a cyclic hexapeptide C5a receptor antagonist (PMX205) for 2-3 mo resulted in substantial reduction of pathological markers such as fibrillar amyloid deposits (49-62%) and activated glia (42-68%) in two mouse models of AD. The reduction in pathology was correlated with improvements in a passive avoidance behavioral task in Tg2576 mice. In 3xTg mice, PMX205 also significantly reduced hyperphosphorylated tau (69%). These data provide the first evidence that inhibition of a proinflammatory receptor-mediated function of the complement cascade (i.e., C5aR) can interfere with neuroinflammation and neurodegeneration in AD rodent models, suggesting a novel therapeutic target for reducing pathology and improving cognitive function in human AD patients." @default.
- W2155172987 created "2016-06-24" @default.
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- W2155172987 date "2009-07-15" @default.
- W2155172987 modified "2023-10-10" @default.
- W2155172987 title "Treatment with a C5aR Antagonist Decreases Pathology and Enhances Behavioral Performance in Murine Models of Alzheimer’s Disease" @default.
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- W2155172987 doi "https://doi.org/10.4049/jimmunol.0901005" @default.
- W2155172987 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4067320" @default.
- W2155172987 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19561098" @default.
- W2155172987 hasPublicationYear "2009" @default.
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