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

Grant number: 17/10801-1
Support Opportunities:Regular Research Grants
Duration: May 01, 2018 - April 30, 2020
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Andréa da Silva Torrão
Grantee:Andréa da Silva Torrão
Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

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)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
MACE, RUAN CARLOS DE; LIMA, GABRIELY CRISTINA ALVES; CARDINALI, CAMILA APARECIDA ERREIRAS FERNANDES; GONSALVES, ALISSON CARVALHO; PORTARI, GUILHERME VANNUCCHI; GUERRA-SHINOHARA, ELVIRA MARIA; LEBOUCHER, ANTOINE; JUNIOR, JOSE DONATO; KLEINRIDDERS, ANDREA; TORRAO, ANDREA DA SILVA. Benfotiamine protects against hypothalamic dysfunction in a STZ-induced model of neurodegeneration in rats. Life Sciences, v. 306, p. 13-pg., . (17/10801-1)
MACEDO DE MORAES, RUAN CARLOS; SINGULANI, MONIQUE PATRICIO; DE GONCALVES, ALISSON CARVALHO; PORTARI, GUILHERME VANNUCCHI; TORRAO, ANDREA DA SILVA. Oral benfotiamine reverts cognitive deficit and increase thiamine diphosphate levels in the brain of a rat model of neurodegeneration. Experimental Gerontology, v. 141, . (17/10801-1)

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