Department of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Parkville, VIC, Australia.
Department of Neurodegenerative Disease and Geriatric Psychiatry, University of Bonn, Bonn, Germany.
Immunol Cell Biol. 2020 Jan;98(1):28-41. doi: 10.1111/imcb.12301. Epub 2019 Nov 20.
Alzheimer's disease (AD) is characterized by amyloid beta (Aβ) accumulation, tau pathology and neuroinflammation. Recently, there has been considerable interest in the role of neuroinflammation in directly contributing to the progression of AD. Studies in mice and humans have identified a role for microglial cells, the resident innate immune cells of the central nervous system, in AD. Activated microglia are a key hallmark of the disease and the secretion of proinflammatory cytokines by microglia may result in a positive feedback loop between neurons and microglia, resulting in ongoing low-grade inflammation. Traditionally, the pathways of Aβ production and neuroinflammation have been considered independently; however, recent studies suggest that these processes may converge to promote the pathology associated with AD. Here we review the importance of inflammation and microglia in AD development and effects of inflammatory responses on cellular pathways of neurons, including Aβ generation.
阿尔茨海默病（AD）的特征是淀粉样蛋白β（Aβ）积累、tau 病理学和神经炎症。最近，神经炎症在直接促进 AD 进展中的作用引起了相当大的兴趣。在小鼠和人类中的研究已经确定了小胶质细胞在 AD 中的作用，小胶质细胞是中枢神经系统的固有免疫细胞。活化的小胶质细胞是疾病的一个关键标志，小胶质细胞分泌的促炎细胞因子可能导致神经元和小胶质细胞之间的正反馈循环，导致持续的低度炎症。传统上，Aβ产生和神经炎症的途径被认为是独立的；然而，最近的研究表明，这些过程可能会汇聚在一起，促进与 AD 相关的病理学。在这里，我们回顾了炎症和小胶质细胞在 AD 发展中的重要性，以及炎症反应对神经元细胞途径的影响，包括 Aβ的产生。
