Benfotiamine Fights Cognitive Impairment in Alzheimer's

SHANGHAI, China In an animal model of Alzheimers disease (AD), benfotiamine, a lipid-soluble form of B1, improved cognitive function and reduced amyloid deposition, possibly through thiamine-independent mechanisms (Brain. 2010 May;133(Pt 5):1342-51. DOI: 10.1093/brain/awq069). Researchers from Fudan University noted thiamine-dependent processes are critical in glucose metabolism and have been found to be impaired in AD patients. Benfotiamine, a lipid-soluble form of thiamine, has enhanced bioavailability compared to straight B1; it metabolizes quickly, producing high levels of thiamine pyrophosphate (TPP, the active form of thiamine).

The research team used a mouse model of AD to test the effect of benfotiamine on cognitive impairment and pathology alterations. After a chronic eight-week treatment, the active intervention dose-dependently enhanced the animals spatial memory, and reduced both amyloid plaque numbers and phosphorylated tau levels in the animals cortical areas. The effects were not seen when the researchers used fursultiamine, another lipophilic thiamine derivative, suggesting benfotiamine may exert its effects via thiamine-independent mechanisms, possibly by suppressing glycogen synthase kinase-3 activity.