髓样细胞触发受体2在阿尔茨海默病发病中的作用  

Role of Triggering Receptor Expressed on Myeloid Cells-2 in Pathogenesis of Alzheimer Disease

作　　者：陈建玲[1] 李婷 CHEN Jianling;LI Ting(Department Two of Geriatrics,Shanghai Mental Health Center,Shanghai Jiaotong University School of Medicine ,Shanghai 200030,China;Department of Geriatrics,Shanghai Changning Mental Health Center,Shanghai 200335,China)

机构地区：[1]上海交通大学医学院附属精神卫生中心老年二科,上海200030 [2]长宁区精神卫生中心老年科,上海200335

出　　处：《医学综述》2019年第15期2988-2992,共5页Medical Recapitulate

基　　金：上海市精神卫生中心院级课题(2017-YJ-05);长宁区精神卫生中心院级课题(2017001)

摘　　要：阿尔茨海默病(AD)以老年斑、神经原纤维缠结及显著的突触丢失、脑萎缩和神经元细胞死亡等为特征性病理改变。AD病因及发病机制复杂,目前尚缺乏有效的治疗手段,对AD分子病理机制的探索可能有助于发现新的治疗靶点。髓样细胞触发受体2(TREM2)的基因变异可增加AD的发病风险,小胶质细胞和巨噬细胞中TREM2的缺失会导致凋亡神经元、细胞废物、细菌产物等的吞噬减少,其表达增加会导致上述物质的吞噬增加;TREM2的拷贝数变异可导致TREM2折叠、转运和稳定性受损,从而影响小胶质细胞在β淀粉样蛋白(Aβ)斑块周围的聚集,进而导致Aβ整体结构发生改变。The characteristic pathological changes of Alzheimer′s disease(AD)are senile plaques,neurofibrillary tangles and significant synaptic loss,brain atrophy and neuronal cell death.The etiology and pathogenesis of AD are complex,and there is still a lack of effective treatment,so exploring the molecular pathological mechanism of AD may be helpful to find new therapeutic targets.Current studies have shown that gene mutations in triggering receptor expressed on myeloid cells-2(TREM2)can increase the risk of AD.The deletion of TREM2 in microglia and macrophages will lead to the decrease of phagocytosis of apoptotic neurons,cell waste,bacterial products,etc.;the increased expression of TREM2 will lead to the increase of phagocytosis of these substances;the variation of copy number of TREM2 can lead to its folding,stacking,transport and stability damage.As a result,the aggregation of microglia aroundβamyloid protein(Aβ)plaques is affected,leading to the change of the overall structure of Aβ.

关 键 词：阿尔茨海默病 髓样细胞触发受体2 Β淀粉样蛋白 老年斑 TAU蛋白 

分 类 号：R749.1[医药卫生—神经病学与精神病学]