Oral benfotiamine reverts cognitive deficit and increase thiamine diphosphate levels in the brain of a rat model of neurodegeneration

Autor(es)

Macedo de Moraes, Ruan Carlos ^[1] ; Singulani, Monique Patricio ^[1] ; de Goncalves, Alisson Carvalho ^[2] ; Portari, Guilherme Vannucchi ^[2] ; Torrao, Andrea da Silva ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Sao Paulo - Brazil

^[2] Univ Fed Triangulo Mineiro, Inst Hlth Sci, Dept Nutr, Uberaba, MG - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Experimental Gerontology; v. 141, NOV 2020.
• Citações Web of Science: 1

Resumo

It is well known that patients with Alzheimer's disease (AD) have imbalances in blood thiamine concentrations and lower activity of thiamine-dependent enzymes. Benfotiamine, a more bioavailable thiamine analog, has been proposed as an alternative to counteract these changes related to thiamine metabolism. Thus, our study aimed to analyze the effects of benfotiamine supplementation on brain thiamine absorption, as well as on parameters related to neuronal energy metabolism and disease progression in an experimental model of sporadic AD induced by intracerebroventricular injection of streptozotocin (STZ) in rats. The supplementation with 150 mg/kg of benfotiamine for 30 days increased the concentrations of thiamine diphosphate in the hippocampus and entorhinal cortex. This led to an improvement in mitochondria enzymes and insulin signaling pathway, with inactivation of GSK3 alpha/beta and ERK1/2, which are two tau-kinases related to the progression of AD, which could decrease tau hyperphosphorylation and apoptosis signaling. Besides, we observed an increased amount of Glun2b subunit of NMDA receptors, decreased inflammation, and improvement of cognitive deficit. Together, these results suggest that benfotiamine could be a potential therapeutic approach in the treatment of sporadic AD. (AU)

• Processo FAPESP: 17/10801-1 - Benfotiamina e hormônio tireoideano: influência sobre o metabolismo energético neuronal e a progressão da neurodegeneração em um modelo experimental semelhante à Doença de Alzheimer
• Beneficiário: Andréa da Silva Torrão
• Modalidade de apoio: Auxílio à Pesquisa - Regular