The beneficial effect of exercise against Alzheimer's disease may result from improved brain glucose metabolism

Abstract

The potential of physical exercise as an intervention for Alzheimer’s disease (AD) has been extensively reported. In fact, a number of studies have highlighted improvements in β-amyloid (Aβ) peptide and hyperphosphorylated tau (p-tau) as critical mechanisms in exercise-induced beneficial neurological outcomes. However, no therapeutic management have been proven to be effective in humans. Recent evidence has shown that AD may be a metabolic disease related to glucose metabolic dysfunction in the brain. In this regard, some of the mechanisms responsible for the beneficial effects of physical exercise in the pathology of AD appear to be related to alterations in glucose metabolism. Therefore, we propose that the neuroprotective effect of physical exercise against AD through synergetic improvement in brain glucose metabolism and its pathophysiology. The novel perspective presented here partly explains the failure of Aβ/tau-based therapeutic approaches and provides evidence for brain glucose metabolism as a potential therapeutic target in AD.