Macroscopic Evidence, Mesoscopic Theory and Microscopic Mechanism About Exercise Regulating Alzheimer's Disease

Alzheimer's disease (AD) is a progressive neurodegenerative disease, and there is currently no effective clinical intervention model. Epidemiological studies have found that insufficient physical activity is one of the important controllable risk factors for AD, while regular exercise can prevent and alleviate AD by promoting cognitive function. Based on the macro evidence of exercise intervention in AD patients, this study explored the mesoscopic mechanism of exercise regulating AD symptoms, and further explored the micro mechanism of exercise mediated AD pathology. Macroscopic evidence suggests that exercise can improve brain cognitive function and reduce the risk of AD by improving cardiopulmonary function, cerebral blood flow, brain plasticity, brain cognitive reserve, and inhibiting brain atrophy. In the mesoscopic mechanism, exercise can regulate pathological symptoms of amyloid-β (Aβ) deposition, tau hyperphosphorylation, neuroinflammation, and abnormal energy metabolism in the brain to inhibit the onset of AD. In terms of micro mechanism, exercise intervention can regulate the pathological mechanism of AD by mediating biological molecules such as neurotrophic factors, irisin, kynurenic acid, lactate, ketone bodies, cathepsin B, and related signal pathways.