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.

体育锻炼作为阿尔茨海默病 (AD) 干预措施的潜力已被广泛报道。事实上，许多研究都强调了 β-淀粉样蛋白 (Aβ) 肽和过度磷酸化 tau (p-tau) 的改善是运动诱导的有益神经系统结果的关键机制。然而，没有任何治疗管理被证明对人类有效。最近的证据表明，AD可能是一种与大脑葡萄糖代谢功能障碍有关的代谢疾病。在这方面，一些负责体育锻炼对 AD 病理学有益影响的机制似乎与葡萄糖代谢的改变有关。因此，我们提出体育锻炼对 AD 的神经保护作用是通过协同改善脑葡萄糖代谢及其病理生理学来实现的。