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.
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Rui Bian and Zhang Su are corresponding authors in this study. R.B conceived the hypothesis. R.B and Z.S supervised the study. All authors wrote the manuscript text. All authors read and approved the final manuscript.
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Highlights
- Physical exercise (PE) is a promising non-pharmacological strategy for Alzheimer’s disease (AD) and has been found to increase melatonin levels. This suggests that exercise-induced melatonin may contribute to AD prevention and treatment by reducing amyloid-β (Aβ) accumulation and modulating inflammation.
- It is suggested that exercise and melatonin improve neuroplasticity, regulate Aβ synthesis, and increase Aβ clearance. These findings support the hypothesis that increased melatonin levels caused by exercise may protect against AD by lowering Aβ.
- Future research is encouraged by this review to ascertain the precise mechanisms via which exercise impacts melatonin secretion and how this impacts the clearance of Aβ. It is also important to ascertain the best exercise regimens, melatonin supplementation strategies, and potential synergistic benefits with other anti-AD therapies. To confirm the effectiveness of exercise-induced melatonin in managing and preventing AD, more clinical research is required to assess the long-term impacts and cognitive deterioration in a range of populations.
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Bian, R., Xiang, L. & Su, Z. Harnessing the benefits of physical exercise-induced melatonin: a potential promising approach to combat Alzheimer’s disease by targeting beta-amyloid (Aβ). Hormones (2024). https://doi.org/10.1007/s42000-024-00602-6
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DOI: https://doi.org/10.1007/s42000-024-00602-6