Physical exercise: a multi-target strategy for the prevention and treatment of Alzheimer’s disease
- 1School of Physical Education, Nanchang University , ,
Abstract
Alzheimer’s disease (AD) is a devastating age-related neurodegenerative disease characterized by irreversible cognitive dysfunction and neuronal loss. The complex pathogenesis of AD involves core proteinopathies of amyloid-β (Aβ) and tau, chronic neuroinflammation, and extensive cerebral metabolic disorders, which collectively drive progressive neuronal damage and disease deterioration. Currently, effective disease-modifying drugs for AD are still lacking, and physical exercise has been recognized as a safe and effective non-pharmacological intervention to prevent and alleviate AD pathological progression. Specifically, exercise inhibits abnormal Aβ deposition and tau hyperphosphorylation, suppresses microglial overactivation and sustained neuroinflammatory responses, and remodels cerebral metabolic homeostasis by improving glucose utilization, balancing lactate metabolism, restoring mitochondrial function, and correcting dysregulated lipid metabolism. Additionally, exercise-mediated upregulation of brain-derived neurotrophic factor (BDNF) enhances neuronal survival and synaptic plasticity to block AD pathological progression. This review innovatively combines core AD pathological markers and multi-dimensional metabolic mechanisms, providing a theoretical reference for further exploring the molecular mechanism of exercise intervention in AD.
Related
- Characteristics of treatment responses to physical exercise and diet in diabetic peripheral artery disease patients: a systematic review.
- Vaccination as a Strategy for Cardiovascular Prevention: Closing a Gap in Clinical Practice
- Alzheimer's Disease Neurofibrillary Pathophysiology: PTPRD- and Flavonol-Modified Mechanisms, Prevention and Therapeutics.
- The stress response of the liver to physical exercise
- Editorial: Impacts of physical activity and exercise on metabolic disorders
BibTeX
@article{tong2026physical,
title = {{Physical exercise: a multi-target strategy for the prevention and treatment of Alzheimer’s disease}},
author = {Wuyun Tong},
journal = {Frontiers in aging neuroscience},
year = {2026},
month = oct,
doi = {10.3389/fnagi.2026.1876075},
url = {https://europepmc.org/article/PMC/PMC13725395},
note = {CC BY},
}
RIS
TY - JOUR
TI - Physical exercise: a multi-target strategy for the prevention and treatment of Alzheimer’s disease
AU - Wuyun Tong
PY - 2026
DA - 2026/10/19
JO - Frontiers in aging neuroscience
DO - 10.3389/fnagi.2026.1876075
UR - https://europepmc.org/article/PMC/PMC13725395
AB - Alzheimer’s disease (AD) is a devastating age-related neurodegenerative disease characterized by irreversible cognitive dysfunction and neuronal loss. The complex pathogenesis of AD involves core proteinopathies of amyloid-β (Aβ) and tau, chronic neuroinflammation, and extensive cerebral metabolic disorders, which collectively drive progressive neuronal damage and disease deterioration. Currently, effective disease-modifying drugs for AD are still lacking, and physical exercise has been recognized as a safe and effective non-pharmacological intervention to prevent and alleviate AD pathological progression. Specifically, exercise inhibits abnormal Aβ deposition and tau hyperphosphorylation, suppresses microglial overactivation and sustained neuroinflammatory responses, and remodels cerebral metabolic homeostasis by improving glucose utilization, balancing lactate metabolism, restoring mitochondrial function, and correcting dysregulated lipid metabolism. Additionally, exercise-mediated upregulation of brain-derived neurotrophic factor (BDNF) enhances neuronal survival and synaptic plasticity to block AD pathological progression. This review innovatively combines core AD pathological markers and multi-dimensional metabolic mechanisms, providing a theoretical reference for further exploring the molecular mechanism of exercise intervention in AD.
SN - 1663-4365
ER -