Abstract:

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. 

Key words:

chronic cerebral ischemia, microglia, astrocyte, synaptic pruning, phagocytosis