背景 β淀粉样蛋白（Aβ）在细胞外的异常聚集被认为是引起认知功能损害等临床症状的重要原因之一。小胶质细胞是脑内的主要免疫细胞，细胞外蓄积的Aβ可与小胶质细胞发生固有免疫反应。目的 探讨小胶质细胞在Aβ所致认知功能损害中的作用。内容 细胞外蓄积的Aβ作为损伤相关分子模式可与小胶质细胞发生免疫应答活化小胶质细胞，小胶质细胞有两种激活途径，经典型活化的小胶质细胞（M1）释放IL-1β、IL-6，TNF-α等多种损伤因子介导中枢炎症反应，进而损伤神经元和破坏突触结构，造成学习和记忆功能损害；而替代激活的小胶质细胞（M2），对胞外聚集的Aβ有较强的吞噬清除能力，具有一定的保护作用。活化小胶质细胞的极性受到细胞因子等多种因素的调节，增加M2型小胶质细胞，减少M1小胶质细胞可能是一种有效的治疗干预方法。趋向 目前对调节Aβ活化小胶质细胞M1/M2表型的研究很多，但以体外实验居多，是否对小胶质细胞极性的调控能成为治疗Aβ相关认知损害性疾病的靶点还需要在更多的动物实验中进行研究。
Background Amyloid β(Aβ) proteins can be aggregated and deposited in the extracellular space as plaques, it is well-known that toxic Aβis related to the progression of cognitive impairment. Objective Provide the potential for greater understanding of Aβrelated pathophysiology. Content Microglia could be activated into classic activated state (M1 state) or alternative activated state (M2 state); the former induce neuroinflammation by secreting inflammatory cytokines including IL-1β、IL-6，TNF-α, and the latter is neurotrophic by taking up fibril Aβthrough phagocytosis. Shifting microglial M1 to M2 stateis could be considered to be an effective therapy for Aβrelated cognitive impairment. Trend At present, there are many studies on shifting microglial M1 to M2 states, but mainly in cell experiments. Whether the regulation of microglia polarity can be a target for treatment of Aβ related cognitive impairment also needs to be studied in more animal experiments.
Cited
)
