ArticleNeurochemical research2020
Treadmill Exercise Attenuates Aβ-Induced Mitochondrial Dysfunction and Enhances Mitophagy Activity in APP/PS1 Transgenic Mice.
Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.
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Who cites it
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 55 citations in OpenAlex.
- Effect of exercise on cognitive function and synaptic plasticity in Alzheimer's disease models: A systematic review and meta-analysis.Frontiers in aging neuroscience · 2022Pooled it
- Insights Into Parkin-Mediated Mitophagy in Alzheimer's Disease: A Systematic Review.Frontiers in aging neuroscience · 2021Pooled it
- Exercise and fluoxetine in Alzheimer's disease: Molecular mechanisms of synergistic and antagonistic effects (Review).International journal of molecular medicine · 2026Review
- The Neuroprotective Role of Exercise in Alzheimer's Disease: An Integrative Review of Animal and Human Studies.Neurology international · 2026Review
- Lifestyle strategies and mechanistic implications for slowing neurodegeneration.npj metabolic health and disease · 2026Review
- The impact of exercise on brain mitochondrial health and its relevance to Alzheimer's disease.Brain and environment · 2026Article
- Regulation of autophagy-mediated pathways by diet, physical activity, and sleep in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Chronic Exercise Protects Against Cognitive Deficits in an Alzheimer's Disease Model by Enhancing Autophagy and Reducing Mitochondrial Abnormalities.Molecular neurobiology · 2025Article
- Exercise training exerts beneficial effects on Alzheimer's disease through multiple signaling pathways.Frontiers in aging neuroscience · 2025Review
- Intervention strategies for Parkinson's disease: the role of exercise and mitochondria.Frontiers in aging neuroscience · 2025Review
- Exercise as a Therapeutic Intervention for Alzheimer's Disease.Advances in neurobiology · 2025Review
- Integrative effects of saffron and physical activity on endurance performance, quality of life, cognitive, emotional, and metabolic outcomes in age-related and neurodegenerative diseases.Frontiers in nutrition · 2025Review
- Exercise Alleviates Fluoride-Induced Learning and Memory Impairment in Mice: Role of miR-206-3p and PREG.Biological trace element research · 2024Article
- Article
- Lactate Mediates High-Intensity Interval Training-Induced Promotion of Hippocampal Mitochondrial Function through the GPR81-ERK1/2 Pathway.Antioxidants (Basel, Switzerland) · 2023Article
- Analysis of Effect of Intensity of Aerobic Exercise on Cognitive and Motor Functions and Neurotrophic Factor Expression Patterns in an Alzheimer's Disease Rat Model.Journal of personalized medicine · 2023Article
- Engineered macrophage-biomimetic versatile nanoantidotes for inflammation-targeted therapy against Alzheimer's disease by neurotoxin neutralization and immune recognition suppression.Bioactive materials · 2023Article
- Mitophagy regulation in aging and neurodegenerative disease.Biophysical reviews · 2023Review
- Defective mitophagy and the etiopathogenesis of Alzheimer's disease.Translational neurodegeneration · 2022Review
- Promise of irisin to attenuate cognitive dysfunction in aging and Alzheimer's disease.Ageing research reviews · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction is a hallmark of Alzheimer's disease (AD), which may be related to mitophagy failure. Previous reports suggest that treadmill exercise protects against mitochondrial dysfunction in AD. However, few studies have investigated the relationship between mitophagy and mitochondrial adaptation caused by treadmill exercise in AD. The current study aimed to investigate whether exercise-ameliorated AD is associated with changes in mitophagy activity. Both Wild-type and APP/PS1 transgenic mice were divided into sedentary (WTC and ADC) and exercise (WTE and ADE) groups (n = 9 for each group). WTE and ADE mice were subjected to treadmill exercise for 12 weeks, followed by evaluating the effect of treadmill exercise on learning and memory ability, Aβ plaques, mitochondrial Aβ peptide level, synaptic activity and mitochondrial function. Meanwhile, mitophagy-related proteins PINK1, Parkin, LC3II and P62 were measured in the hippocampal mitochondrial fractions. The results indicated that exercise not only restored learning and memory ability, but also reduced Aβ plaque area, mitochondrial Aβ peptide level, and increased levels of synaptic markers SYN and GAP43, as well as reversed mitochondrial dysfunction (defective mitochondrial ultrastructure, decreased PGC-1α, TFAM and ATP levels) in APP/PS1 transgenic mice. Moreover, exercise increased mitophagy activity as evidenced by a significant decrease in levels of P62 and PINK1 as well as an increase in levels of LC3II and Parkin in ADE mice. These findings suggest that treadmill exercise can enhance mitophagy activity in the hippocampus, which is efficient in ameliorating pathological phenotypes of APP/PS1 transgenic mice.
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Registered trials
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