慢性脑缺血又称慢性脑低灌注，是造成以脑白质损伤和认知功能减退为主要表现的多种中 枢神经系统疾病的重要原因。已有研究表明，持续性慢性脑缺血会引起小胶质细胞的异常激活，导致髓鞘 再生障碍和突触过度丢失。在正常的神经系统发育过程中，小胶质细胞可通过补体 3/补体 1q/补体受体 3 （complement 3/complement 1q/complement receptor 3，C3/C1q/CR3）和趋化因子 C⁃X3⁃C⁃基序配体 1/C⁃X3⁃C⁃基 序受体 1（C⁃X3⁃C motif chemokine ligand 1/C⁃X3⁃C motif chemokine receptor 1，CX3CL1/CX3CR1）信号通路等 多种分子机制吞噬多余的突触，介导突触修剪。然而，在包括慢性脑缺血在内的多种中枢神经系统疾病 中，调控突触修剪的这些分子机制异常，引起小胶质细胞吞噬功能受损或过度激活，导致突触异常堆积或 丢失，最终引起认知功能障碍。本文综述了小胶质细胞在慢性脑缺血后介导的突触异常修剪的相关分子 机制，为治疗慢性脑缺血所致的认知功能障碍寻找潜在的靶点。

Chronic cerebral ischemia，also known as chronic cerebral hypoperfusion，is a major cause of various central nervous system diseases with main manifestations of white matter injury and cognitive decline. Per⁃ sistent cerebral hypoperfusion has been shown to induce abnormal activation of microglia，resulting in impairment of myelin regeneration and excessive loss of synapses. During brain development，microglia can associate with multiple molecular mechanisms，such ascomplement 3/complement 1q/complement receptor 3（C3/C1q/CR3）or the C⁃X3⁃C motif chemokine ligand 1/C⁃X3⁃C motif chemokine receptor 1（CX3CL1/ CX3CR1）signaling pathway to engulf the redundantsynapses and mediate synaptic elimination. However，among a variety of central nervous system diseases including chronic cerebral ischemia，the abnormalities of the above molecular mechanisms often lead to the altered microglial phagocytosis，which ultimately results inaccumulation or loss of synapses and cogni⁃ tive dysfunction. This paper reviews the researches intothe roles and mechanisms of microglia ⁃ mediated synaptic elimination after chronic cerebral ischemia so as to look for a potential target for treating cognitive declines induced by chronic cerebral ischemia.