小胶质细胞
神经炎症
发病机制
β淀粉样蛋白
神经科学
趋化因子
神经退行性变
淀粉样蛋白(真菌学)
医学
免疫学
炎症
阿尔茨海默病
淀粉样β
特雷姆2
老年斑
中枢神经系统
疾病
生物
病理
作者
Zhiyou Cai,Muhammad Delwar Hussain,Yan Lv
标识
DOI:10.3109/00207454.2013.833510
摘要
Compelling evidence from basic molecular biology has demonstrated the dual roles of microglia in the pathogenesis of Alzheimer's disease (AD). On one hand, microglia are involved in AD pathogenesis by releasing inflammatory mediators such as inflammatory cytokines, complement components, chemokines, and free radicals that are all known to contribute to beta-amyloid (Aβ) production and accumulation. On the other hand, microglia are also known to play a beneficial role in generating anti-Aβ antibodies and stimulating clearance of amyloid plaques. Aβ itself, an inducer of microglia activation and neuroinflammation, has been considered as an underlying and unifying factor in the development of AD. A vicious cycle of inflammation has been formed between Aβ accumulation, activated microglia, and microglial inflammatory mediators, which enhance Aβ deposition and neuroinflammation. Thus, inhibiting the vicious cycle seems to be a promising treatment to restrain further development of AD. With increasing research efforts on microglia in AD, intervention of microglia activation and neuroinflammation in AD may provide a potential target for AD therapy in spite of the provisional failure of nonsteroidal antiinflammatory drugs in clinical trials.
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