Exercise Enhances SIRT1 Expression and Improves Alzheimer’s Disease / 中国生物化学与分子生物学报

ABSTRACT

Alzheimer’s disease (AD) is a neurodegenerative disease, β-amyloid (Aβ) deposition and Tau protein hyperphosphorylation are the main pathological features. Silent mating-type information regulation 2 homolog 1 (SIRT1) can deacetylate various types of histones and non-histones, and play an important role in the pathogenesis of AD. Recent studies found that exercise can activate SIRT1 to delay the progression of AD. The mechanisms may be as follows inhibit the activity of β-secretase and increase the activity of α-secretase to reduce the production of Aβ; reduce the accumulation of hyperphosphorylated Tau protein; interact with PGC-1α to promote mitochondrial biogenesis; up-regulate PINK1/ Parkin signaling pathway to improve mitochondrial autophagy; and deacetylate NF-κB to inhibit neuroinflammation. In addition, the protein levels of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) in hippocampus are increased, and ApoE4 gene is inhibited to enhance synaptic plasticity. This article summarizes the role and mechanisms of exercise in improving AD by regulating SIRT1, and provides new ideas for the prevention and treatment of AD.