Background Exercise induces neuroprotection; it can reduce age‐related decline and may be used as an alternative therapeutic nondrug strategy for neurodegenerative diseases, yet the exact molecular mechanism through which exercise protects the brain has not been fully understood. The following study investigated the effects of exercise on mitochondria‐mediated apoptosis in the prevention of Alzheimer’s disease (AD). Methods and Results Male wild‐type mice and transgenic APP/PS1 mice were divided into the wild‐type sedentary group, wild‐type exercise group, transgenic APP/PS1 sedentary group, and transgenic APP/PS1 exercise group. The mice in exercise groups were subjected to treadmill training for 12 weeks. A 12 week treadmill exercise reduced the percentage of TUNEL‐positive cells in the hippocampal dentate gyrus (DG) region, decreased the levels of β‐amyloid (Aβ) and Aβ‐binding alcohol dehydrogenase (ABAD) in the hippocampus, alleviated the mitochondrial fragmentation, reduced the activity of reactive oxygen species (ROS), increased the level of adenosine triphosphate (ATP), and reduced the levels of mitochondrial apoptosis‐related proteins in the hippocampus of APP/PS1 mice. Conclusions This data suggest that exercise may help prevent AD by regulating mitochondria‐mediated apoptosis.
Li et al. (2026) studied this question.