Affiliations: [a] Research Master’s Programme Brain and Cognitive Sciences, University of Amsterdam, Amsterdam, The Netherlands | [b] Neurotrack Technologies Inc., Redwood City, CA, USA
| [c] Clinical Excellence Research Center, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA
| [d] Department of Psychology, PGSP-Stanford Consortium, Palo Alto University, Palo Alto, CA, USA
Correspondence:
[*]
Correspondence to: Nicholas T. Bott, Clinical Excellence Research Center, Department of Medicine, Stanford
University School of Medicine, 75 Alta Road, Stanford, CA 94305, USA. Tel.: +1 650 814 9383;
E-mail: nbott@stanford.edu.
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.
