Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019;69(2):311-338.
doi: 10.3233/JAD-180958.

Prevention and Treatment of Alzheimer's Disease: Biological Mechanisms of Exercise

Affiliations
Review

Prevention and Treatment of Alzheimer's Disease: Biological Mechanisms of Exercise

Hugo McGurran et al. J Alzheimers Dis. 2019.

Abstract

Alzheimer's disease (AD) is the most common form of dementia. With an aging population and no disease modifying treatments available, AD is quickly becoming a global pandemic. A substantial body of research indicates that lifestyle behaviors contribute to the development of AD, and that it may be worthwhile to approach AD like other chronic diseases such as cardiovascular disease, in which prevention is paramount. Exercise is an important lifestyle behavior that may influence the course and pathology of AD, but the biological mechanisms underpinning these effects remain unclear. This review focuses on how exercise can modify four possible mechanisms which are involved with the pathology of AD: oxidative stress, inflammation, peripheral organ and metabolic health, and direct interaction with AD pathology. Exercise is just one of many lifestyle behaviors that may assist in preventing AD, but understanding the systemic and neurobiological mechanisms by which exercise affects AD could help guide the development of novel pharmaceutical agents and non-pharmacological personalized lifestyle interventions for at-risk populations.

Keywords: Aging; Alzheimer’s disease; amyloid; cardiovascular; exercise; inflammation; insulin; oxidative stress; tau.

PubMed Disclaimer