Oral benfotiamine reverts cognitive deficit and increase thiamine diphosphate levels in the brain of a rat model of neurodegeneration.
Level 5 - mechanism / opinion, no new human data
Preclinical animal model (rodent study)
PubMed 32987117 · doi:10.1016/j.exger.2020.111097
What was done
Researchers administered oral benfotiamine (150 mg/kg daily for 30 days) to a rat model of sporadic Alzheimer's disease induced by intracerebroventricular injection of streptozotocin. They evaluated brain thiamine absorption (thiamine diphosphate concentrations in the hippocampus and entorhinal cortex), mitochondrial enzyme activity, insulin signaling pathways, tau-kinase activation (GSK3α/β and ERK1/2), NMDA receptor GluN2B subunits, inflammation, and cognitive performance.
What was found
The abstract reports directional outcomes without numerical data, effect sizes, or p-values. Benfotiamine supplementation increased thiamine diphosphate in the hippocampus and entorhinal cortex, improved mitochondrial enzyme activity and insulin signaling, inactivated the tau-kinases GSK3α/β and ERK1/2, increased GluN2B subunit expression, reduced inflammation, and reversed cognitive deficits.
Why it matters
This study provides preclinical evidence that a highly bioavailable thiamine derivative can penetrate relevant brain regions and counteract several metabolic, kinase-mediated, and cognitive deficits in a neurodegenerative model.
Limits
The study was conducted entirely in a chemically induced rodent model (intracerebroventricular streptozotocin), which does not fully capture human Alzheimer's disease biology. The abstract does not report the total sample size (n), precise quantitative measurements, variance, or statistical significance metrics. The intervention was evaluated over a single 30-day period with one dose level.
Cited by
- contradicts Benfotiamine is converted into a water-soluble form in the blood and does not cross the blood-brain barrier effectively.