脂联素在运动调节自噬并缓解阿尔茨海默病过程中的效应及机制  

Effects of adiponectin on exercise-induced autophagy in Alzheimer disease

作　　者：简晔 刘文锋[1,2] 袁顺灵 JIAN Ye;LIU Wen-feng;YUAN Shun-ling(Hunan Provincial Key Laboratory of Physical Fitness and Sports Rehabilitation,Hunan Normal University,Changsha 410012,China;The Key Laboratory of Protein Chemistry and Developmental Biology of Ministry of Education,Hunan Normal University,Changsha 410081,China)

机构地区：[1]湖南师范大学体适能与运动康复湖南省重点实验室,湖南长沙410012 [2]湖南师范大学蛋白质化学与发育生物学教育部重点实验室,湖南长沙410081

出　　处：《中国病理生理杂志》2022年第1期154-161,共8页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.81702236);湖南教育厅重点项目(No.20A333);湖南省高校青年骨干教师项目(湘教通[2020]43号);湖南省自然科学基金项目(No.2018JJ3363);湖南省研究生科研创新项目资助(No.CX20210481)。

摘　　要：阿尔茨海默病(Alzheimer disease,AD)是一种神经系统退行性疾病,常称为老年性痴呆,由德国神经病理学家Alois Alzheimer发现。大多数研究认为AD的发病机制主要有tau蛋白假说、β-淀粉样蛋白(amyloidβ-protein,Aβ)瀑布学说、胆碱能学说、氧化应激学说和神经炎性假说等[1]。Adiponectin(APN)is a protein hormone produced and secreted exclusively by adipocytes,with multiple physiological functions,such as reducing insulin resistance,anti-inflammation,anti-oxidation,as well as participating in and regulating the occurrence and development of cognitive impairment. It has been reported that APN and its receptors(AdipoR)are correlated with autophagy in Alzheimer disease(AD). Exercise not only regulates autophagy,but also affects the expression of APN and AdipoR. Recently,the effects of exercise-induced autophagy on impaired cognitive function have been explored. Exercise promotes the expression of APN and AdipoR as well as regulating autophagy. We propose a possible molecular mechanism that exercise regulates autophagy in AD through APN-AdipoR1 pathways.

关 键 词：运动 阿尔茨海默病 脂联素 自噬 

分 类 号：R749.16[医药卫生—神经病学与精神病学] R363[医药卫生—临床医学]