阿尔茨海默病（Alzheimer's disease，AD）常见于老年人，临床表现为记忆力减退、精神行为异常等。 AD的发病机制目前尚不清楚，目前存在的多种假说并不能完全解释AD的全部发病特征。小胶质细胞是脑 组织中特殊的巨噬细胞，可监测周围神经元和胶质细胞的健康情况，同时具有神经保护和神经毒性作用。 近年来通过对AD的不断深入研究发现，小胶质细胞通过髓系细胞触发受体2（triggering receptor expressed on myeloid cells 2，TREM2）参与AD发病机制，TREM2功能丧失会加剧AD的发展进程。本文就TREM2及 其突变体介导小胶质细胞功能改变在AD发生发展中的作用进行综述。

Alzheimer's disease (AD), commonly observed in the elderly, manifests clinically with symptoms such as memory decline and neuropsychiatric abnormalities. The pathogenesis of AD remains unclear to date, as the various existing hypotheses fail to fully account for all the disease characteristics of AD. Microglia, specialized macrophages in brain tissue, monitor the health of surrounding neurons and glial cells, exhibiting both neuroprotective and neurotoxic effects. Recent in-depth research on AD has revealed that microglia participate in the pathogenesis of AD through the triggering receptor expressed on myeloid cells 2 (TREM2). Loss of TREM2 function exacerbates the progression of AD. This article reviews the role of TREM2 and its mutants in mediating microglial functional alterations during the occurrence and development of AD.