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- W2027323660 endingPage "9" @default.
- W2027323660 startingPage "1" @default.
- W2027323660 abstract "Neuroinflammation is involved in the pathogenesis of Alzheimer's disease (AD). Microglia, macrophage-like resident immune cells in the brain, play critical roles in the inflammatory aspects of AD. Microglia may be activated by oligomeric and fibrillar species of amyloid β (Aβ) that are constituents of senile plaques and by molecules derived from degenerated neurons, such as purines and chemokines, which enhance their migration and phagocytosis. The main neurotoxic molecules produced by activated microglia may be reactive oxygen species, glutamate, and inflammatory cytokines such as tumor-necrosis-factor-α and interleukin- (IL-) 1β These molecules differentially induce neurotoxicity. Aβ itself directly damages neurons. In terms of neuroprotective properties, microglia treated with fractalkine or IL-34 attenuate Aβ neurotoxicity by Aβ clearance and the production of antioxidants. Therefore, regulation of the microglial role in neuroprotection may be a useful therapeutic strategy for AD." @default.
- W2027323660 created "2016-06-24" @default.
- W2027323660 creator A5069337032 @default.
- W2027323660 date "2012-01-01" @default.
- W2027323660 modified "2023-10-16" @default.
- W2027323660 title "The Biphasic Role of Microglia in Alzheimer's Disease" @default.
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