阿尔茨海默病的内质网应激机制与运动干预研究进展  

Research Progress of Endoplasmic Reticulum Stress Mechanism and Exercise Intervention in Alzheimer’s Disease

作　　者：夏杰[1,2] 赵娜[1,2] 王璟[1,2] 徐波[1,2] XIA Jie;ZHAO Na;WANG Jing;XU Bo(Key Laboratory of Adolescent Health Assessment and Exercise Intervention,Ministry of Education,East China Normal University,Shanghai 200241,China;College of Physical Education and Health,East China Normal University,Shanghai 200241,China)

机构地区：[1]华东师范大学“青少年健康评价与运动干预”教育部重点实验室,上海200241 [2]华东师范大学体育与健康学院,上海200241

出　　处：《中国体育科技》2020年第9期20-29,共10页China Sport Science and Technology

基　　金：国家自然科学基金项目(31571225)。

摘　　要：阿尔茨海默病(Alzheimer’s disease,AD)是一种神经退行性疾病,主要以Tau蛋白过度磷酸化和β淀粉样蛋白聚集,以及突触损伤为病理特征,其中内质网应激(endoplasmic reticulum stress,ERS)所诱发的未折叠蛋白反应(unfolded protein response,UPR)过度激活是介导AD病理的重要机制之一。研究表明,适宜的运动能够调节神经细胞ERS和抑制AD的多种病变,但其确切机制尚不清楚。通过分析ERS与AD病理和运动干预之间的关系,发现运动可通过抑制ERS,减少异常磷酸化Tau蛋白和Aβ聚集,提高突触可塑性和自噬活性等途径缓解AD,其机制可能是运动促进能量代谢适应,改善蛋白质折叠和质量监控的内质网环境,减轻ERS,从而防止错误折叠蛋白质的产生和突触相关蛋白表达紊乱。Alzheimer’s disease(AD)is a disorder of protein homeostasis characterized by Tau protein hyperphosphorylation,beta-amyloid protein deposition and inhibition of synaptic-related protein synthesis.Endoplasmic reticulum is responsible for correctly folding or processing newly synthesized proteins,and ER stress is induced when misfolded or unfolded proteins are accumulated.Recently,increasing evidence has demonstrated that the ER stress is implicated in the pathogenesis of AD.Exercise can regulate ERS and inhibit various pathological changes of AD,but the specific mechanism is still unclear.According to the research,the relationships between ERS and Tau pathology,Aβ,synaptic plasticity,autophagy and exercise are extensively analyzed,aiming to inspire new ideas for the treatment of AD.

关 键 词：阿尔茨海默病 运动 内质网应激 

分 类 号：G804.2[文化科学—运动人体科学]