Research Progress on the Potential Mechanisms of Exercise Regulating BDNF Expression to Improve Alzheimer’s Disease
LEI Senlin, CHEN Ping, CHEN Xiaoan*
AD (Alzheimer’s disease) is a prevalent neurodegenerative condition marked by progressive memory impairment, cognitive deficits, behavioral and psychological symptoms, and the eventual loss of executive abilities, which collectively degrade the quality of life for affected individuals. BDNF (brain-derived neurotrophic factor) as a crucial endogenous neuroprotective factor, is an effective regulator of related pathogenic factors in the occurrence and development of AD, but its expression is abnormally down-regulated in the course of AD. Exercise therapy, an efficacious, non-pharmacological strategy for AD prevention and intervention, has been shown to enhance BDNF expression via the myokine irisin, with the OCN (osteocalcin) also potentially contributing to BDNF regulation. Aerobic, resistance, and cognitive-motor exercises can promote the expression of BDNF to a certain extent, thereby inducing its neuroprotective effects and subsequently improving symptoms associated with AD. The potential mechanisms of exercise in improving AD by regulating BDNF encompass the reduction of Aβ (amyloidbeta) aggregation, inhibition of Tau hyperphosphorylation, mitigation of neuroinflammation, and amelioration of synaptic plasticity impairment. This article delves into the role of BDNF in the pathogenesis of AD, scrutinizing the mechanisms by which exercise modulates BDNF expression within the AD pathological context. It specifically focuses on the beneficial effects of various exercise interventions targeting BDNF in AD, and explores the underlying mechanisms through which exercise may delay the onset and progression of AD. This study aims to furnish novel theoretical insights and perspectives for the therapeutic application of exercise in AD.
CN
EN