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.

中文翻译：

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先天性免疫应答和神经炎症在阿尔茨海默氏病淀粉样蛋白积累和进展中的作用。

阿尔茨海默氏病（AD）的特征在于淀粉样β（Aβ）积累，tau病理和神经炎症。最近，人们对神经炎症在直接促进AD进展中的作用引起了极大的兴趣。在小鼠和人类中的研究已经确定了小胶质细胞的作用，小胶质细胞是中枢神经系统的固有先天免疫细胞。活化的小胶质细胞是该疾病的关键标志，小胶质细胞分泌促炎细胞因子可能会导致神经元和小胶质细胞之间形成正反馈回路，从而导致持续的轻度炎症。传统上，Aβ产生和神经炎症的途径被独立考虑；但是，最近的研究表明，这些过程可能会融合以促进与AD相关的病理。