Effect of resistance exercise in female transgenic mice for Alzheimer's disease

• Grant number: 22/08264-6
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): December 01, 2022
• Effective date (End): July 31, 2023
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Beatriz de Oliveira Monteiro
• Grantee: Emilly Vitória Figueiredo Santos
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

AAlzheimer's disease (AD) is clinically characterized by progressive memory loss, behavioral and learning dysfunction, and cognitive deficits. Its main pathological features are the increase of ²-amyloid plaques (²‘) and neurofibrillary tangles of tau protein, as well as changes in microglial cells and cortisol levels. For the experimental study of AD, experimental models were developed in transgenic animals with ²‘ plaque production. Among them are the double transgenic mice APPswe/PS1dE9 (APP/PS1), which are widely used in several studies in AD, with the formation of ²‘ plaques that begin to be detectable in the cortex and hippocampus starting at six months of age, in addition to cognitive deficits and memory impairment. Several studies, both in patients with AD and in animals, have shown the positive impact of physical exercise on individuals diagnosed with AD. Physical exercise may delay the process of neurodegeneration in AD, as well as reduce the risks of developing the disease. However, most studies use aerobic exercise, and few studies have investigated the effects of other modalities that may also have positive effects on AD, such as resistance exercise (RE). Studies have identified mechanisms by which RE contributes to improve cognitive deficit, and to reduce A² load and neuroinflammation.Thus, the present study aims to investigate the effects RE on behavioral changes in memory and locomotor activity, on the ²‘ plaque formation, on corticosterone levels (stress) and on the modulation of the microglial activation observed in AD in APP/PS1 transgenic female mice.