With advancements in our ability to treat or manage more diseases than ever, people are able to live longer in greater health. However, for individuals who develop Alzheimer's disease (AD), therapeutic options are currently limited to symptom management or have minimal impact on underlying disease mechanisms. The effectiveness of available treatments also diminishes as the disease progresses. Therefore, it is critical that interventions are implemented in early stages of disease to prevent the establishment of pathological features and to delay or prevent cognitive decline that can severely lower quality of life. Regular exercise is known to reduce the risk of, and may slow the progression of AD. A significant portion of the known benefits of exercise are likely due to the modification of cardiometabolic risk factors, which are associated with AD. However, the mechanism by which exercise might confer neuroprotective benefits, specific to the pathology of AD, are not well understood. This review examines the effect of exercise on several biochemical pathways, focusing on their convergence at ‘a disintegrin and metalloproteinase-10′ as a mediator capable of delaying the progression of Alzheimer's disease.