ArticleJournal of exercise rehabilitation2015
Treadmill exercise decreases incidence of Alzheimer's disease by suppressing glycogen synthase kinase-3β expression in streptozotocin-induced diabetic rats.
Article in Journal of exercise rehabilitation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Exercise training exerts beneficial effects on Alzheimer's disease through multiple signaling pathways.Frontiers in aging neuroscience · 2025Review
- Comparing prophylactic effect of exercise and metformin on cognitive brain functions in rats with type 3 diabetes mellitus.Archives of medical science : AMS · 2024Article
- From Obesity to Hippocampal Neurodegeneration: Pathogenesis and Non-Pharmacological Interventions.International journal of molecular sciences · 2020Review
- Mechanisms of Aerobic Exercise Upregulating the Expression of Hippocampal Synaptic Plasticity-Associated Proteins in Diabetic Rats.Neural plasticity · 2019Article
- Sweet Mitochondria: A Shortcut to Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2018Review
- Treadmill exercise improves motor and memory functions in cerebral palsy rats through activation of PI3K-Akt pathway.Journal of exercise rehabilitation · 2017Article
- Treadmill exercise ameliorates Alzheimer disease-associated memory loss through the Wnt signaling pathway in the streptozotocin-induced diabetic rats.Journal of exercise rehabilitation · 2016Article
- Characterization of prefrontal cortex microstructure and antioxidant status in a rat model of neurodegeneration induced by aluminium chloride and multiple low-dose streptozotocin.Metabolic brain disease · 2015Article
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Authors and funding
5 authors at 5 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Diabetes is a metabolic disorder, and it is considered as a major risk factor for Alzheimer's disease (AD). In the present study, we evaluated whether treadmill exercise ameliorates progression of AD in relation with glycogen synthase kinase-3β (GSK-3β) activity using streptozotocin (STZ)-induced diabetic rats. For this study, step-down avoidance task, immunohistochemistry for glycogen synthase kinase-3β (GSK-3β) and tau, and western blot for phosphor-phosphoinositide 3 kinase (p-PI3K)/PI3K and phosphor-Akt (p-Akt)/Akt were performed. Diabetes mellitus was induced by intraperitoneal injection of STZ. The rats in the exercise groups were made to run on the treadmill for 30 min per one day, five times a week, during 12 weeks. The present results showed that short-term and long-term latencies in the step-down avoidance task were decreased by induction of diabetes, and treadmill exercise inhibited these latencies in the diabetic rats. Induction of diabetes suppressed the ratio of p-PI3K to PI3K and the ratio of p-Akt to Akt, and treadmill exercise increased these ratios in the diabetic rats. The numbers of GSK-3β-positive and tau-positive cells in the hippocampal dentate gyrus was higher in the diabetes-induction group than that in the control group, and treadmill exercise inhibited these numbers in the diabetic rats. In the present study, treadmill exercise suppressed hyperphosphorylation of tau in the hippocampus by decreased GSK-3β activity through PI3K/Akt pathway activation in the diabetic rats. Based on the present results, treadmill exercise may helpful to prevent diabetes-associated AD occurrence.
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