Benfotiamine and thyroid hormone: influence on neuronal energy metabolism and neurodegeneration progression in an experimental model similar to Alzheimer's Disease

Abstract

Alzheimer's Disease (AD) is the most common form of dementia in elderly people, and is characterized by neuronal degeneration of regions related to cognitive functions. Its etiology is still unknown and age is the major risk factor, but genetic and environmental factors seem to contribute to the development and progression of the disease. Studies suggest that disturbances in glucose metabolism and insulin signaling in the brain are associated with the early stages and progression of AD. In this context, AD may be a result of decreased glucose metabolism and mitochondrial function in the brain, with decreased expression and enzyme activity and lower activity of the electron transport chain. Thus, the search for therapeutic strategies that may interfere with mitochondrial function and improve the metabolism of glucose in the nervous system is extremely important.The aim of this study is to evaluate the effects of supplementation of benfotiamine (a synthetic analogue of thiamine, vitamin B1) and thyroid hormone triiodotyronine (T3), molecules related to metabolism and mitochondrial function, in an experimental model of neurodegeneration that mimics some aspects of AD (intracerebroventricular injection of streptozotocin) in rats.After the supplementation period, the animals will be evaluated for their cognitive performance in the object recognition behavioral test and for biochemical and molecular parameters such as thiamine dosage, mitochondrial enzyme activity, and protein and gene expression related to mitochondrial activity and neurodegeneration markers. (AU)