ArticleMolecular neurobiology2025
Benfotiamine Ameliorates Streptozotocin-Induced Alzheimer's Disease in Rats by Modulating Neuroinflammation, Oxidative Stress, and Microglia.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Brain-Targeting siRNA Delivery to Tackle Alzheimer's Disease.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnologyReview
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Authors and funding
5 authors.
Funding
Abstract
Alzheimer's disease (AD) is the most prevalent cause of dementia, characterized by progressive memory loss and cognitive decline. Recent evidence indicates that inflammation plays a central role in AD pathogenesis, with elevated inflammatory markers and risk genes linked to innate immune functions. Glial cell dysfunction, particularly in astrocytes and microglia, is crucial to the neuroinflammatory process, contributing to oxidative stress, synaptic dysfunction, neuronal death, and impaired neurogenesis. This study aimed to investigate the therapeutic effects of benfotiamine (BFT), a vitamin B1 analogue, on microglial morphology, inflammation, and oxidative stress parameters in a sporadic Alzheimer-like disease model induced by intracerebroventricular injection of streptozotocin (STZ). Supplementation with 150 mg/kg of BFT for 7 days significantly reduced inflammation in the hippocampus and provided protection against oxidative damage in the entorhinal cortex by activating the Nrf-2 pathway and enhancing the expression of antioxidant enzymes such as SOD1 and CAT. These findings suggest that BFT exerts neuroprotective effects in AD, particularly impacting glial cell function and redox homeostasis.
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Registered trials
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