ArticleNeurochemical research2025
Treadmill Exercise Alleviates Neuroinflammation, Demyelination, and Apoptosis Induced by Hyperactivation of Microglia in the Hippocampus of Senescent Mice by Regulating the SIRT1/PPARγ Pathway.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Voluntary Exercise and Hippocampal Memory Enhancement: Decoding the Molecular Blueprint.Journal of molecular neuroscience : MN · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
Cognitive dysfunction is a major feature of brain aging. However, there is no effective treatment for brain aging. Aerobic exercise is a non-side-effective intervention that is effective in neurodegenerative diseases such as aging. The aim of this study was to explore the potential of treadmill exercise in preventing oxidative stress-induced brain aging and neurodegenerative diseases by investigating the effects of treadmill exercise and its mechanisms in D-galactose-induced mice. The results showed that D-galactose-induced C57BL/6 mice exhibited cognitive deficits, myelin deficits, and increased neuronal apoptosis. Additionally, we observed significantly elevated average optical density values of IBA-1, a microglia-specific marker, in the senescent group. These were effectively mitigated following the treadmill exercise. The study also found that treadmill exercise increased the expression of Silent Information Regulator 1 (SIRT1) and Peroxisome proliferator-activated receptor γ (PPARγ) proteins, while decreasing the expression of p-NFKB. Immunofluorescence double-labeling further validated that SIRT1 and PPARγ co-localized and that treadmill exercise contributed to increased SIRT1 and PPARγ overlapping fluorescence intensity. Treadmill exercise decreased the expression of IL-1β and iNOS, and decreased the number of TUNEL-positive cells and the expression of the apoptosis executor caspase3. The results suggest that aerobic exercise has the potential to ameliorate the cognitive deficits observed in D-galactose mice by modulating the SIRT1/PPARγ signaling pathway to impede microglia-induced neuroinflammation and reduce apoptosis. Treadmill exercise appears to have the potential to be an effective treatment for attenuating microglia inflammation-induced brain aging and neurodegenerative diseases.
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Registered trials
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