小胶质细胞吞噬β淀粉样蛋白及毒性机制的研究进展  

Research Progress in Phagocytosis and Toxicity Mechanism of Microglia toβ-Amyloid

作　　者：马艳冬 刘航[1] 王艺璇 石镜明[1] MA Yandong;LIU Hang;WANG Yixuan;SHI Jingming(Neurodegenerative Diseases and Tibetan Medicine Intervention Research Laboratory,School of Medicine,Xizang Minzu University,Xianyang 712082,China)

机构地区：[1]西藏民族大学医学院神经退行性疾病与藏药干预研究实验室,陕西咸阳712082

出　　处：《医学综述》2023年第13期2509-2512,2519,共5页Medical Recapitulate

基　　金：国家自然科学基金(32160215)。

摘　　要：阿尔茨海默病(AD)严重危害老年人的身心健康,但其发病机制目前尚未明确,β淀粉样蛋白(Aβ)与小胶质细胞相互作用可能是其主要风险因素之一。髓系细胞触发受体2与Aβ及脂蛋白形成的复合体结合可导致Aβ被吞噬或清除,同时小胶质细胞的表型和功能也会发生改变,导致大量炎症因子释放,从而产生神经炎症,直接损伤神经元,导致AD发生。因此,深入研究小胶质细胞吞噬Aβ的具体机制,可以为有效防治AD提供新思路。Alzheimer′s disease(AD)is a serious threat to the physical and mental health of the elderly,but its pathogenesis is still unclear.The interaction betweenβ-amyloid(Aβ)and microglia may be one of the main risk factors.The complex formed by triggering receptor expressed on myeloid cells 2 with Aβand lipoprotein can lead to the phagocytosis or clearance of Aβ.At the same time,the phenotype and function of microglia will also change,resulting in the release of a large number of inflammatory factors,thus generating neuroinflammation,directly damaging neurons and leading to the occurrence of AD.Therefore,in-depth study of the specific mechanism of microglia phagocytosis of Aβcan provide new ideas for effective prevention and treatment of AD.

关 键 词：Β淀粉样蛋白 小胶质细胞 细胞受体 神经炎症 

分 类 号：R518.4[医药卫生—内科学]