Harnessing the benefits of physical exercise-induced melatonin: a potential promising approach to combat Alzheimer's disease by targeting beta-amyloid (Aβ).

Abstract

Alzheimer's disease (AD) is a chronic neurogenerative disease that impairs cognition, learning, behavior, and memory. The aberrant accumulation of extracellular amyloid-β (Aβ) plaques is a characteristic of AD. It has been demonstrated that melatonin exerts a significant role in AD prevention and treatment via its antioxidant effects, reducing neuroinflammation, and Aβ. Moreover, studies have shown that physical exercise (PE) is not only a promising non-pharmacological strategy for AD prevention and treatment but can also lead to an increase in melatonin levels. Hence, we hypothesized that PE can contribute to AD prevention and treatment by increasing melatonin levels and reducing Aβ accumulation, enhancing Aβ clearance, and modulating inflammation in these patients. However, the mechanisms by which PE increases melatonin synthesis and the cellular and molecular mechanisms of actions of melatonin in AD prevention and treatment have not to date been completely understood. Therefore, in the future, further investigations are required to elucidate the underlying mechanisms, optimize intervention strategies, identify biomarkers, and validate findings through clinical trials. Understanding the potential of exercise-induced melatonin in AD holds promise for innovative therapeutic interventions and future directions in AD research.