ArticleMetabolic brain disease2025
Aerobic exercise and metformin attenuate the cognitive impairment in an experimental model of type 2 diabetes mellitus: focus on neuroinflammation and adult hippocampal neurogenesis.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Role of the NLRP3 inflammasome in diabetes and its complications (Review).Molecular medicine reports · 2025Review
- From Diabetes to Degenerative Diseases: The Multifaceted Action of Metformin.International journal of molecular sciences · 2025Review
- Electroacupuncture ameliorates cognitive dysfunction in T2DM rats by modulating astrocytic polarization and aberrant energy metabolism in the hippocampus via the Wnt/β-catenin pathway.Diabetology & metabolic syndrome · 2025Article
- Young apple polyphenol extract prevents diabetic cognitive dysfunction by promoting TET2-mediated active DNA demethylation in the brain of diabetic mice.Frontiers in nutrition · 2025Article
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Authors and funding
4 authors.
Funding
Abstract
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder that increases the prevalence of cognitive impairment in the geriatric population. Aerobic exercise is an excellent non-pharmacological therapeutic strategy to prevent Alzheimer's disease, the most common form of dementia. The exact molecular mechanism of aerobic exercise (Exe) as an intervention to counter cognitive decline is far from clear. Metformin is a first-line agent against T2DM with neuroprotective properties. The present study assessed the role of treadmill exercise in combination with a low dose of metformin (Met; 70 mg/kg) in cognitive impairment and its associated molecular mechanism in T2DM rats. The experimental model of T2DM-associated cognitive decline was created by administration of a high-fat diet (HFD) with a low dose of streptozotocin (STZ; 35 mg/kg). Neurobehavioral assessments were performed to evaluate spatial recognition and fear-conditioned memory across the groups: control, HFD + STZ, HFD + STZ + Exe, and HFD + STZ + Exe + Met. In addition, we performed immunohistochemistry and western blotting on the rat hippocampal tissue from the above groups for protein expression studies. T2DM rats showed a significant cognitive decline compared to the control group, which improved in the long-term exercise and metformin co-administered animals. The level of neuroinflammation was significantly elevated in the hippocampal tissue of T2DM rats compared to the control and lowered after exercise and metformin treatment. T2DM reduced mature neurons and neurogenesis while increasing astrogliosis and microgliosis, ameliorated by exercise and metformin treatment. Moreover, T2DM impaired hippocampal neurogenesis by reducing the canonical Wnt/β-catenin pathway, which got upregulated in exercise and metformin-co-administered rats. Long-term aerobic exercise with metformin treatment ameliorated neuroinflammation and promoted adult hippocampal neurogenesis via upregulating the canonical Wnt/β-catenin pathway in T2DM rats.
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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 Socratic graph.