Study summary · research use only
Evaluation of neuroprotective role of benfotiamine in Alzheimer's disease model: A randomized control study
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat study, the authors examined benfotiamine (BFT), a lipid-soluble thiamine derivative, in an aluminium chloride (AlCl3)-induced model of Alzheimer's disease (AD). Rats received AlCl3 for one month to induce dementia; a positive control group received donepezil, and BFT groups received 50 and 300 mg/kg body weight per day for the last 15 days. AlCl3 was reported to significantly impair learning and memory and to increase acetylcholine esterase, caspase 8, and tau proteins. The decrease in nitric oxide was highly significant in BFT-treated rats versus control (p<0.001), lower-dose BFT increased glutathione levels (p=0.012), and higher-dose BFT was associated with improved learning and memory (p=0.009) and reduced markers of taupathy and apoptosis. The authors state further validation by clinical trial is needed.
Abstract
Thiamine deficiency mimics the features of Alzheimer's disease (AD) like cognitive impairment, amyloid and tau deposition. There is growing evidence that links AD with aluminium. The study aims to explore the effect of benfotiamine (BFT), a lipid soluble thiamine derivative, on aluminium induced AD rat model. All the rats except control group were administered AlCl3 for one month to induce dementia. Positive control group received donepezil; BFT groups received 50 and 300 mg/kg b.w. /day for last 15 days. Morris water maze test was performed to assess learning and memory. Histological changes were studied in C3 region of hippocampus. Acetylcholine esterase (AChE), malondialdehyde, reduced glutathione, nitric oxide, hyperphosphorylated tau proteins and caspase 8 were estimated in brain homogenate. AlCl3 impaired learning and memory significantly and increased AChE, caspase 8, tau proteins. The decrease in NO level was highly significant (p<0.001) in BFT treated rats compared to control. Lower dose of BFT had profound influence on augmenting GSH levels (p=0.012). Further, higher dose of BFT improved learning and memory significantly in AD model (p=0.009) and was more effective in preventing taupathy, apoptosis and neuronal damage by acting as a potent antioxidant. It can be concluded that oral supplementation of 300mg /kg b.w. /day of BFT may reverse AD pathological processes and improve dementia. However, the need of thiamine supplementation in elderly persons to delay or halt the cognitive loss and eventual dementia needs validation by clinical trial.
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