自噬与神经营养因子在运动干预阿尔茨海默病中的作用

Role of autophagy and neurotrophic factors in exercise intervention in Alzheimer’s disease

阿尔茨海默病(AD)是一种以渐进性记忆障碍为主要临床表现的神经退行性疾病。在临床药物无法根治的现状下,运动干预带来的良好效应为治疗指引了新的方向。运动通过抑制mTOR信号传导通路、刺激内质网应激、加速线粒体损伤消除等自噬调节方式或加速β淀粉样蛋白、tau蛋白的消除,或减弱它们的生成。同时,运动还对神经元的凋亡起着调节作用。它提高了BDNF、NGF等神经营养因子,激活了PI3-k/Akt途径,抑制了caspase-3和COX-2等凋亡因子的活性,从而减缓神经元的凋亡,减慢AD的进程。

Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive memory impairment as the main clinical manifestation and treatment of the disease is still a challenge to clinical medicine. The positive effect by exercise intervention brings a potential direction of treatment. It has been found that exercise either accelerates the beta amyloid(Aβ), tau protein elimination, or diminishes their production by inhibiting the mTOR signaling pathway, stimulation of endoplasmic reticulum stress, accelerated mitochondrial damage and other regulatory mechanisms of autophagy. At the same time, exercise also plays a role in regulating the apoptosis of neurons. It improves the neurotrophic factors such as BDNF and NGF, activates the pathway of PI3-k/Akt and inhibits the activity of apoptosis factors such as caspase-3 and COX-2, thus slows down neuronal apoptosis and slows down the progression of AD.