ArticleLife (Basel, Switzerland)2023
Aerobic Exercise Delays Alzheimer's Disease by Regulating Mitochondrial Proteostasis in the Cerebral Cortex and Hippocampus.
Article in Life (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- Molecular mechanisms underlying exercise-enhanced autophagy in improving neuroplasticity in Alzheimer's disease.Frontiers in aging neuroscience · 2026Review
- β-amyloid and β-amyloid precursor protein synthesis and processing: effects of exercise and exercise-related injury.Frontiers in cellular neuroscience · 2026Review
- Exercise attenuates the hallmarks of aging: Novel perspectives.Journal of sport and health science · 2025Review
- Gene-Exercise Interactions in Amyloid Metabolism and Clearance: Implications for Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Mitophagy in perioperative neurocognitive disorder: mechanisms and therapeutic strategies.European journal of medical research · 2025Review
- Creatine supplementation and exercise in aging: a narrative review of the muscle-brain axis and its impact on cognitive and physical health.Frontiers in nutrition · 2025Review
- Cellular senescence in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2024Review
- From Plaques to Pathways in Alzheimer's Disease: The Mitochondrial-Neurovascular-Metabolic Hypothesis.International journal of molecular sciences · 2024Review
- Honokiol relieves hippocampal neuronal damage in Alzheimer's disease by activating the SIRT3-mediated mitochondrial autophagy.CNS neuroscience & therapeutics · 2024Article
- The Role of Endothelial Cell Mitophagy in Age-Related Cardiovascular Diseases.Aging and disease · 2024Review
- 8-weeks aerobic exercise ameliorates cognitive deficit and mitigates ferroptosis triggered by iron overload in the prefrontal cortex ofFrontiers in neuroscience · 2024Article
- Physical exercise for brain plasticity promotion an overview of the underlying oscillatory mechanism.Frontiers in neuroscience · 2024Review
- Development of brain organoid technology derived from iPSC for the neurodegenerative disease modelling: a glance through.Frontiers in molecular neuroscience · 2023Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In clinical practice, Alzheimer's disease (AD), as one of the main neurodegenerative diseases globally, currently has no cure. Recently, the delaying and improving effects of physical exercise on AD have gradually been confirmed; however, the specific mechanism involved needs further clarification. (1) Objective: Explore the mechanism aerobic exercise plays in delaying AD by regulating mitochondrial proteostasis and provide new theoretical bases for improving and delaying AD through aerobic exercise in the future. (2) Methods: Male APP/PS1 mice were randomly divided into a normal group (NG, n = 20), activation group (AG, n = 20), and inhibition group (SG, n = 20). Then, the mice in each group were randomly divided into control group and exercise group (n = 10 mice each), yielding the normal control group (CNG), normal exercise group (ENG), active control group (CAG), active exercise group (EAG), inhibitive control group (CSG), and inhibitive exercise group (ESG). After adaptive training, the mice in the exercise groups were trained on an aerobic treadmill for 12 weeks; we conducted behavioral tests and sampled the results. Then, quantitative real-time PCR (Q-PCR) and Western blot analysis were performed. (3) Results: In the Morris water maze (MWM) test, the latency was significantly reduced and the number of platform crossings was significantly increased in the CAG and ENG compared with the CNG, while the result of the CSG was contrary to this. Compared with the ENG, latency was significantly reduced and the number of platform crossings was significantly increased in the EAG, while the opposite occurred for ESG. Compared with the CAG, the latency was significantly reduced and the number of platform crossings was significantly increased in the EAG, while the results for CSG were contrary. In the step-down test, compared with the CNG, the latency was significantly increased and the number of errors was significantly reduced in the CAG and ENG, respectively, while the results for CSG were contrary. Compared with the ENG, the latency was significantly increased and the number of errors was significantly reduced in the EAG, while the results for ESG were contrary. Compared with the CAG, the latency was significantly increased and the number of errors was significantly reduced in the EAG, while the results for CSG were contrary. Mitochondrial unfolded protein reactions (UPR
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.