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.
Keywords: Alzheimer’s disease; Amyloid precursor protein; Exercise; β-Amyloid peptide.
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.