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Neural and behavioral evaluation during the aging of transgenic mice submitted to gestational protein restriction: investigation of Alzheimer's Disease-related proteins

Grant number: 21/04333-0
Support type:Scholarships in Brazil - Doctorate
Effective date (Start): June 01, 2021
Effective date (End): May 31, 2023
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal researcher:Jose Antonio Rocha Gontijo
Grantee:Vinícius Schiavinatto Mariano
Home Institution: Faculdade de Ciências Médicas (FCM). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Associated research grant:13/07607-8 - OCRC - Obesity and Comorbidities Research Center, AP.CEPID

Abstract

In the last decades life expectancy has increased dramatically, leading to a growing global elderly population and implying challenges for public health in develop new strategies to promote healthy aging to this population. The increase and prevalence of chronic Non-Communicable Diseases (NCDs), including cardiovascular diseases, obesity, and metabolic diseases, may lead to increased susceptibility to dementia and neurodegenerative diseases, such as Alzheimer's Disease (AD), directly interfering in the healthy aging and quality of life of these individuals. Adverse events during embryo-fetal ontogenesis, such as malnutrition, can lead to adaptations in the fetus, predisposing the individual to NCDs, and to behavioral and neuropsychiatric disorders, such as anxiety and depression in later life. Furthermore, studies have shown that the accumulation of beta-amyloid and intracellular tau protein characteristic of AD, as well as neural senescence, are associated with dysfunctions in neural autophagy, promoting progressive cognitive decline. Thus, aiming to understand the effects of gestational malnutrition on neural aging of offspring, this project aims to evaluate sensory and motor activity, spatial memory and learning, anxiety, fear and depression; neural senescence, autophagic dynamics, and hippocampal AD markers during aging in female and male transgenic mice (C57BL/6-CAG-RFP-EGFP-LC3) submitted to gestational protein restriction. The identification of these mechanisms may lead to the establishment of a natural model for the study of AD, enabling the investigation of the etiology of late-onset/sporadic AD. (AU)

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