Abstract：
Microglia are the resident brain macrophage cells that are involved in constant surveillance of brain microenvironment. In Alzheimer\'s disease, microglia get over activated upon the accumulation of Tau and amyloid-β species in the extracellular space, ultimately leading to neurodegeneration. Microglia phagocytose the extracellular Tau species by several mechanisms among which P2Y12 receptor-mediated internalization of extracellular Tau is recently studied. Extracellular Tau activates microglia and directly interacts with the P2Y12 receptor. Tau-receptor complex is then internalized followed by perinuclear accumulation and lysosomal degradation. Upon microglial activation by extracellular Tau, P2Y12 receptor is also involved in membrane-associated actin remodeling which has its key role in active migration and phagocytosis.
摘要：
小胶质细胞是参与持续监测脑微环境的固有脑巨噬细胞。在阿尔茨海默病中，小胶质细胞在细胞外空间中Tau和淀粉样蛋白-β的积累后被激活，最终导致神经变性.小胶质细胞通过几种机制吞噬细胞外Tau物种，其中最近研究了P2Y12受体介导的细胞外Tau内化。细胞外Tau激活小胶质细胞并直接与P2Y12受体相互作用。然后将Tau受体复合物内化，然后进行核周积累和溶酶体降解。在细胞外Tau激活小胶质细胞后，P2Y12受体还参与膜相关肌动蛋白重塑，在主动迁移和吞噬作用中起关键作用。
