ArticleJournal of exercise nutrition & biochemistry2015
Effect of treadmill exercise on PI3K/AKT/mTOR, autophagy, and Tau hyperphosphorylation in the cerebral cortex of NSE/htau23 transgenic mice.
Article in Journal of exercise nutrition & biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- A meta-analysis of the efficacy of physical exercise interventions on activities of daily living in patients with Alzheimer's disease.Frontiers in public health · 2024Pooled it
- Exercise-induced GPLD1 is associated with neuroprotection and improvement of hippocampal dysfunction in an Alzheimer's disease model.Metabolic brain disease · 2026Article
- Mechanistic advances in exercise‑mediated regulation of autophagy dysfunction in Alzheimer's disease (Review).International journal of molecular medicine · 2026Review
- 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
- Article
- Molecular mechanisms underlying exercise-enhanced autophagy in improving neuroplasticity in Alzheimer's disease.Frontiers in aging neuroscience · 2026Review
- Specific regulation of muscle protein metabolism in broilers by dietary fermented cottonseed meal.Frontiers in veterinary science · 2026Article
- Exercise-driven cellular autophagy: A bridge to systematic wellness.Journal of advanced research · 2025Review
- [Mechanisms of spinal microglia and astrocytes in exercise-induced analgesia].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- Peripheral immune and metabolic regulation of Aβ and Tau by exercise in Alzheimer's disease.Frontiers in immunology · 2025Review
- Exercise training exerts beneficial effects on Alzheimer's disease through multiple signaling pathways.Frontiers in aging neuroscience · 2025Review
- Changes in the hippocampal level of tau but not beta-amyloid may mediate anxiety-like behavior improvement ensuing from exercise in diabetic female rats.Behavioral and brain functions : BBF · 2024Article
- Leptin Signaling Could Mediate Hippocampal Decumulation of Beta-Amyloid and Tau Induced by High-Intensity Interval Training in Rats with Type 2 Diabetes.Cellular and molecular neurobiology · 2023Article
- Article
- Recent advances on the molecular mechanisms of exercise-induced improvements of cognitive dysfunction.Translational neurodegeneration · 2023Review
- Does Exercise Regulate Autophagy in Humans? A Systematic Review and Meta-Analysis.Autophagy reports · 2023Review
- Precious but convenient means of prevention and treatment: physiological molecular mechanisms of interaction between exercise and motor factors and Alzheimer's disease.Frontiers in physiology · 2023Review
- Treadmill exercise promotes E3 ubiquitin ligase to remove amyloid β and P-tau and improve cognitive ability in APP/PS1 transgenic mice.Journal of neuroinflammation · 2022Article
- The Effects of Six Weeks of Endurance Training and CGRP Inhibition on Nrf2 and AKT Expression in the Hippocampal Tissue of Male Wistar Rats.Mediators of inflammation · 2022Article
- Exercise Cuts Both Ways with ROS in Remodifying Innate and Adaptive Responses: Rewiring the Redox Mechanism of the Immune System during Exercise.Antioxidants (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeNeurofibrillary tangles, one of pathological features of Alzheimer's disease, are produced by the hyperphosphorylation and aggregation of tau protein. This study aimed to investigate the effects of treadmill exercise on PI3K/AKT/mTOR signal transmission, autophagy, and cognitive ability that are involved in the hyperphosphorylation and aggregation of tau protein.
methodsExperimental animals (NSE/htau23 mice) were divided into non-transgenic control group (Non-Tg-Control; CON; n = 7), transgenic control group (Tg-CON; n = 7), and transgenic exercise group (Tg-Treadmill Exercise; TE; n = 7). The Tg-TE group was subjected to treadmill exercise for 12 weeks. After the treadmill exercise was completed, the cognitive ability was determined by conducting underwater maze tests. Western blot was conducted to determine the phosphorylation status of PI3K/AKT/mTOR proteins and autophagy-related proteins (Beclin-1, p62, LC3-B); hyperphosphorylation and aggregation of tau protein (Ser199/202, Ser404, Thr231, PHF-1); and phosphorylation of GSK-3β, which is involved in the phosphorylation of tau protein in the cerebral cortex of experimental animals.
resultsIn the Tg-TE group that was subjected to treadmill exercise for 12 weeks, abnormal mTOR phosphorylation of PI3K/AKT proteins was improved via increased phosphorylation and its activity was inhibited by increased GSK-3β phosphorylation compared with those in the Tg-CON group, which was used as the control group. In addition, the expression of Beclin-1 protein involved in autophagosome formation was increased in the Tg-TE group compared with that in the Tg-CON group, whereas that of p62 protein was reduced in the Tg-TE group compared with that in the Tg-CON group. Autophagy was activated owing to the increased expression of LC3-B that controls the completion of autophagosome formation. The hyperphosphorylation and aggregation (Ser199/202, Ser404, Thr231, PHF-1) of tau protein was found to be reduced in the Tg-TE group compared with that in the Tg-CON group. Furthermore, in the underwater maze test, the Tg-TE group showed a reduced escape time and distance compared with those of the Tg-CON group, suggesting that learning and cognitive ability were improved.
conclusionThese findings suggest that aerobic exercise such as treadmill exercise might be an effective approach to ameliorate the pathological features (or neurofibrillary tangles) of Alzheimer's disease.
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