ArticleScientific reports2025
Vanadyl sulfate restores memory impairment in streptozotocin-induced rat model of sporadic alzheimer's disease by repressing FoxO1 gene expression.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Chasing the FoxO in Metabolic Disorders: Novel Considerations for Oxidative Stress, Programmed Cell Death, Wnt, and the Gut Microbiome.Antioxidants (Basel, Switzerland) · 2026Review
- Osteoarthritis and dementia: contrasting disorders driven by mutual pathways of autophagy, mTOR, GLP-1, AMPK, Wnt, and WISP1.Expert review of clinical pharmacology · 2026Review
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
- Agitation, Alzheimer's disease, and autophagy: mechanistic insights into aging pathways, gut microbiome, and artificial intelligence.Frontiers in immunology · 2026Review
- Cannabis and Cannabidiol: Pioneering Treatment for the Nervous System with Alzheimer's Disease and Peripheral Organ Involvement with Nonalcoholic Fatty Liver Disease (NAFLD).Current neurovascular research · 2025Article
- Dementia, mood disorders, and aging: Bridging new avenues of care through shared biological pathways.Aging advancesArticle
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4 authors.
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Abstract
Impaired brain insulin signaling is a risk factor for the pathogenesis of Alzheimer's disease (AD). FoxO1 and HMGA1 transcription factors are involved in the pathogenesis of both type 2 diabetes (T2D) and Alzheimer's disease (AD). This study aimed to assess the effect of vanadyl sulfate (VS) on impaired memory and hippocampal FoxO1 and HMGA1 RNA expression in sporadic AD (sAD) model in rats. Thirty-two male Wistar rats (250 ± 10 g) were divided into sham, AD, and VS 0.5 and 0.75 treated groups. The animals were subjected to two bilateral intracerebroventricular (icv) injections of either citrate buffer or streptozotocin (STZ) at 72-hour intervals. The VS-treated groups were treated with either 0.5 or 0.75 mg/ml oral VS for 3 weeks. The target quadrant entry latency, path length, and time and distance traveled in the target quadrants were assessed with the Morris water maze (MWM). Hippocampal tissues were analyzed for FoxO1 and HMGA1 RNA expressions. Group differences and group‒time interactions were analyzed via mixed two-way repeated-measures ANOVA. VS treatment in icv STZ rats restored impaired spatial memory. Hippocampal FOXO1 and HMGA1 RNA expressions were significantly lower in VS-treated and sham groups compared to AD control. VS can restore impaired spatial memory in sAD rats, possibly via the repression of FoxO1 and HMGA1 RNA expression in hippocampus.
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