Neuroprotective mechanisms of chronic physical exercise via reduction of β-amyloid protein in experimental models of Alzheimer's disease: A systematic review.

Abstract Aims Alzheimer's disease (AD) is the most common irreversible chronic neurodegenerative disease. It is characterized by the abnormal accumulation of β-amyloid protein (Aβ), which triggers homeostatic breakage in several physiological systems. However, the effect of chronic exercise on the formation of Aβ as an alternative therapy has been investigated. This systematic review examines the antiamyloid effect of different types and intensities of exercise, seeking to elucidate its neuroprotective mechanisms. Main methods The research was conducted in the electronic databases Pubmed, Embase, Scopus and Web of Science, using the following descriptors: “amyloid beta” (OR senile plaque OR amyloid plaque) and “exercise” (OR physical activity OR training). The risk of bias was evaluated through SYRCLE's Risk of Bias for experimental studies. Key findings 2268 articles were found, being 36 included in the study. A higher frequency of use of mice with genetic alterations was identified for the Alzheimer's disease (AD) model (n = 29). It was used as chronic training: treadmill running (n = 24), voluntary running wheel (n = 7), swimming (n = 4) and climbing (n = 2). The hippocampus and the cortex were the most investigated regions. However, physiological changes accompanied by the reduction of Aβ and associated with AD progression were verified. It is concluded that exercise reduces the production of Aβ in models of animals with AD. Significance Nevertheless, this effect contributes to the improvement of several physiological aspects related to Aβ and that contribute to neurological impairment in AD.