Alzheimer’s disease (AD) is associated with a very large burden on global healthcare systems. Thus, it is imperative to find effective treatments of the disease. One feature of AD is the accumulation of neurotoxic β-amyloid peptide (Aβ). Aβ induces multiple pathological processes that are deleterious to nerve cells. Despite the development of medications that target the reduction of Aβ to treat AD, none has proven to be effective to date. Non-pharmacological interventions, such as physical exercise, are also being studied. The benefits of exercise on AD are widely recognized. Experimental and clinical studies have been performed to verify the role that exercise plays in reducing Aβ deposition to alleviate AD. This paper reviewed the various mechanisms involved in the exercise-induced reduction of Aβ, including the regulation of amyloid precursor protein cleaved proteases, the glymphatic system, brain-blood transport proteins, degrading enzymes and autophagy, which is beneficial to promote exercise therapy as a means of prevention and treatment of AD and indicates that exercise may provide new therapeutic targets for the treatment of AD.

阿尔茨海默病 (AD) 与全球医疗保健系统的巨大负担有关。因此，寻找有效的治疗方法势在必行。AD 的一个特征是神经毒性 β-淀粉样肽 (Aβ) 的积累。Aβ 诱导多种对神经细胞有害的病理过程。尽管开发了靶向降低 Aβ 来治疗 AD 的药物，但迄今为止没有一种药物被证明是有效的。非药物干预，如体育锻炼，也在研究中。运动对 AD 的益处已得到广泛认可。已经进行了实验和临床研究，以验证运动在减少 Aβ 沉积以减轻 AD 中的作用。本文回顾了运动引起的 Aβ 减少的各种机制，