运动调节神经细胞自噬改善阿尔茨海默病

Autophagy is an essential degradation pathway in clearing abnormal protein aggregates from mammalian cells and is responsible for protein homeostasis and neuronal health. Several studies have shown that autophagy deficits occurred in the brain of Alzheimer's disease (AD). Defects in autophagy affect the metabolism of β-amyloid (Aβ), assembling of Tau, and synaptic plasticity, contributing to the progress of AD. Recently, increasing evidence suggests that aerobic exercise could regulate autophagy, and ameliorate the pathological features of AD animals, but the molecular mechanisms are still unknown. In this review, we summarized the latest progress supporting the role of exercise regulated autophagy in the prevention and treatment of Alzheimer' s disease. Firstly, exercise induces autophagy by activating AMPK and inhibiting mTOR signaling. Exercise enhances autophagy flux and autolysosome degradation, which accelerates the removal of Aβ and phosphorylated Tau. Secondly, Exercise increases the amount of BDNF in the brain, which suppresses autophagy flux via the BDNF/TrkB signaling and the PI3K/Akt pathway, thereby promoting synaptic plasticity and memory through a BDNF-regulated mechanism. In addition, exercise may also maintain neurotransmitter homeostasis by regulating autophagy.