内质网应激在阿尔茨海默病中的研究进展  

Research Progress of Endoplasmic Reticulum Stress in Alzheimer’s Disease

作　　者：钱峰 陈长兰[1] 

机构地区：[1]辽宁大学药学院,辽宁 沈阳

出　　处：《药物资讯》2021年第1期38-45,共8页Pharmacy Information

摘　　要：阿尔茨海默病(Alzheimer’s Disease, AD)是一种起病隐匿的慢性进行性神经性疾病。临床表现为不同程度的记忆力减退和认知功能障碍。目前,对阿尔茨海默病的发病机制以及防治仍然是当前的研究热点。内质网应激(endoplasmic reticulum stress, ERS)是细胞针对外界刺激而做出的一种保护性反应。近年来已有许多研究报道,内质网应激始终贯穿于阿尔茨海默病的发生发展中。阿尔茨海默病中β-淀粉样蛋白(amyloid beta, Aβ)和磷酸化Tau的过度积累都能刺激内质网应激的发生,继而激活未折叠蛋白反应(unfolded protein response, UPR),持续、严重的内质网应激反应则会导致细胞凋亡的发生。因此笔者就针对近年来内质网应激在阿尔茨海默病发病及防治中的作用机制及研究进展做一综述。Alzheimer’s disease (Alzheimer’s Disease, AD) is an insidious onset chronic progressive neurological disorders. The clinical manifestations are varying degrees of memory loss and cognitive dysfunction. At present, the pathogenesis and prevention of Alzheimer’s disease are still the hotspots of research. Endoplasmic reticulum stress (ERS) is a protective response of cells to external stimuli. In recent years, many studies have reported that endoplasmic reticulum stress has always run through the occurrence and development of Alzheimer’s disease. The excessive accumulation of β-amyloid (Aβ) and phosphorylated Tau in Alzheimer’s disease can stimulate the occurrence of endoplasmic reticulum stress, which in turn activates the unfolded protein response (UPR), and continues severe endoplasmic reticulum stress will result in apoptosis. Therefore, the author reviews the mechanism and research progress of endoplasmic reticulum stress in the pathogenesis and prevention of AD in recent years.

关 键 词：阿尔茨海默病 内质网应激 未折叠蛋白反应 Aβ淀粉样蛋白 磷酸化TAU蛋白 

分 类 号：R74[医药卫生—神经病学与精神病学]