配对免疫球蛋白样受体B（paired immunoglobulin like receptor B, PirB）调节突触可塑性作用被认为是造成认知功能障碍的重要原因之一，在中枢神经系统中，过表达的PirB通过增加神经元的凋亡来抑制神经元的存活。文章探讨了PirB抑制中枢神经损伤后轴突生长的机制，分析了PirB在神经退行性疾病、创伤性脑损伤和脑卒中等认知功能相关性疾病中发挥的重要致病作用，阐述了通过选择性阻断PirB功能，干预PirB相关通路所致的认知功能障碍。
Regulating synaptic plasticity by paired immunoglobulin like receptor B (PirB) is considered to be one of the essential causes of cognitive dysfunction. In the central nervous system, overexpression of PirB can cause death of neurons by increasing apoptosis of neurons. This review aims to discuss the mechanism of PirB in inhibiting axonal growth after central nervous system injury and to elucidate the essential pathogenic role of PirB in neurodegenerative diseases, traumatic brain injury and stroke, and other cognitive function‑related diseases. By regulating selective blocking of PirB function, people can intervene the cognitive dysfunction caused by PirB related pathways.
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