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- W2088721908 abstract "Alzheimer's disease (AD) brains contain large numbers of amyloid-beta peptide (Abeta) deposits associated with activated microglia, astrocytes and dystrophic neurites. Activated complement components and pro-inflammatory cytokines are also present, indicative of focal inflammation. However, neither Abeta, nor the chemokine-like mediator, C5a, which is generated by Abeta-mediated complement activation, significantly activates microglia, as assessed by pro-inflammatory cytokine release. We evaluated the possibility that both together would co-stimulate such release using the THP-1 human monocytic cell line as a microglial surrogate, and found this to be the case. These studies support the hypothesis that Abeta and C5a induce a chronic microglia-mediated focal inflammatory response in AD." @default.
- W2088721908 created "2016-06-24" @default.
- W2088721908 creator A5020624931 @default.
- W2088721908 creator A5042418157 @default.
- W2088721908 date "2000-09-01" @default.
- W2088721908 modified "2023-09-30" @default.
- W2088721908 title "The C5a complement activation peptide increases IL-1β and IL-6 release from amyloid-β primed human monocytes: implications for Alzheimer’s disease" @default.
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- W2088721908 doi "https://doi.org/10.1016/s0165-5728(00)00291-5" @default.
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