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Assessment of the influence of mild chronic intermittent cold exposure on the core body temperature, cognitive function, and phosphorylated Tau and BAG2 levels in familial and sporadic mouse models of Alzheimer's Disease

Grant number: 16/01836-3
Support type:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): November 01, 2016
Effective date (End): October 31, 2017
Field of knowledge:Biological Sciences - Physiology - General Physiology
Principal researcher:Maria Camila Almeida
Grantee:Robson Cristiano Lillo Vizin
Supervisor abroad: Andrej A. Romanovsky
Home Institution: Centro de Ciências Naturais e Humanas (CCNH). Universidade Federal do ABC (UFABC). Ministério da Educação (Brasil). Santo André , SP, Brazil
Research place: St. Joseph's Hospital and Medical Center, United States  
Associated to the scholarship:13/25503-5 - Involvement of TRPM8 channels in thermoregulation of Wistar rats, BP.DR


Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disease, accepted to be caused likely due to genetic and/or environmental factors. Loss of memory is one of the earliest clinical symptoms. AD can be classified into late-onset sporadic (SAD) or early-onset familial (FAD) that corresponds only to 1% of cases, and both are histopathologically characterized by amyloid plaques, composed of beta-amyloid deposition, and neurofibrillary tangles formed from hyperphosphorylation of tau protein. Some important risk factors are suggested to SAD such as diabetes mellitus, aging, anesthesia and hypothermia. In fact, a relation between aging and alteration in core body temperature (Tc) homeostasis, as well as the influence of cold- and anesthesia-induced hypothermia on tau phosphorylation and promoting cognitive deficits has been reported by several studies. Moreover, control of Tc in anesthetized old mice can abolish tau hyperphosphorylation and partially recover memory impairment induced by hypothermia. Recently, the co-chaperone BAG2, a protein described to degrade phosphorylated tau, has allowed a new insight for possible pharmacological targets. In this project, 3xTgAD-mice, an FAD model that shown age-dependent increase in Tc similar to that exhibited by AD patients, and intracerebroventricular-streptozotocin mice, a SAD model, will be used to evaluate the influence of chronic intermittent cold exposure (CIC) on Tc, cognitive function using passive avoidance learning and Barnes maze, and phosphorylated tau and BAG2 protein levels by western blot. The use of these two animal models of AD will allow a better comprehension of the relation between temperature, BAG2 protein levels and DA, which will help drive future studies for the development of new medicines for this disease. (AU)

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