随着人口老龄化加剧，神经退行性疾病发病率持续攀升，成为全球公共卫生的重大挑战。髓系细胞 触发受体2（triggering receptor expressed on myeloid cells 2，TREM2）作为小胶质细胞特异性表达的免疫调 节受体，通过调控吞噬功能、炎症反应及细胞代谢，在神经退行性疾病中呈现双重调控作用。TREM2能够 识别受损神经元和病理蛋白（如β-淀粉样蛋白），激活下游PI3K/Akt等信号通路，驱动小胶质细胞向抗炎表 型极化，清除毒性物质并维持神经元代谢稳态；其基因突变可导致蛋白功能异常，显著增加阿尔茨海默病风 险。本文详细综述TREM2在不同神经退行性疾病，尤其是阿尔茨海默病中的作用机制，旨在为未来开发基 于TREM2的治疗方案提供理论依据和新的思路。

As global population aging intensifies, the rising incidence of neurodegenerative diseases poses a significant public health challenge. TREM2 (triggering receptor expressed on myeloid cells 2), an immune regulatory receptor specifically expressed in microglia, plays a dual role in neurodegenerative diseases by modulating phagocytosis, inflammatory responses, and cell metabolism. TREM2 can recognize damaged neurons and pathological proteins, such as β-amyloid. It then activates downstream signaling pathways like PI3K/Akt, driving microglia to an anti-inflammatory phenotype. This process clears toxic substances and maintains neuronal metabolic homeostasis. However, TREM2 gene mutations can lead to abnormal protein function, substantially increasing Alzheimer’s disease risk. This paper comprehensively reviews TREM2’s role in various neurodegenerative diseases, particularly in Alzheimer’s disease, aiming to underpin the development of TREM2-based therapies with theoretical evidence and novel insights.