摘要
阿尔茨海默症是一种与年龄有关的神经退行性疾病,其病理改变主要表现为β-淀粉样蛋白沉积形成的老年斑以及过度磷酸化tau蛋白积聚引起的神经纤维缠结。综述了近期研究成果,发现运动可以提高正常鼠脑内细胞自噬水平,延缓衰老过程中大鼠脑细胞自噬水平的下降,提高AD鼠脑细胞的自噬水平。其机制如下:运动可以激活PI3K/Akt/m TOR信号通路诱导细胞自噬的启动,加快自噬体的形成,促进自噬体与溶酶体的结合,使脑细胞能够快速的通过自噬系统来清除β-淀粉样蛋白和过度磷酸化tau蛋白,进而起到预防和缓解AD的作用。
Alzheimer＇s disease（AD） is an age-related neurodegenerative disease, characterized by extracellular plaque deposits of the β-amyloid peptide and intracellular accumulation of hyperphosphorylated tau protein as neurofibrillary tangles. This paper reviewsthe recent research results showing that exercise not only induces autophagy in heathy rat brain, but also prevents the decline of autophagy activity withage as well as increases autophagy in the brain of AD rats. The possible mechanisms include： exercise activates the PI3 K/Akt/m TOR signaling pathway to initiate the autophagy, which accelerates the formation of autophagosomes, promotes the fusion of autophagosomes and lysosomes,and accelerates the removal of β-amyloid and hyperphosphorylated tau protein through the autophagy system, thus prevents and alleviates the pathology of AD.
作者
赵娜
徐波
张利
李百侠
ZHAO Na1,2, XU Bo1,2, ZHANG Li3, LI Bai-xia2(1 .Key Laboratory of Adolescent Health Assessment and Exercise Intervention o f Ministry o f Education, East China Normal University, Shanghai 200241, China; 2.School of Physical Education ＆ Health Care, East China Normal University, Shanghai 200241; 3.China University of Mining and Technology, Beijing 100083, China)
出处
《中国体育科技》
CSSCI
北大核心
2018年第3期98-104,共7页
China Sport Science and Technology
基金
国家自然科学基金项目(31571225)
