Neurodegenerative diseases, such as Alzheimer's disease (AD), are becoming more common in aging our society. One specific neuropathological hallmark of this disease is excessive accumulation of amyloid-β (Aβ) peptides, which can aggregate to form the plaques commonly associated with this disease. These plaques are often observed well before clinical diagnosis of AD. At the cellular level, both the production and aggregation of Aβ peptides in the brain are detrimental to neuronal cell production, survival, and function, as well as often resulting in neuronal dysfunction and death. Exercise and physical activity have been shown to improve overall health, including brain health, and in the last several years there has been evidence to support that exercise may be able to regulate Aβ peptide production in the brain. Exercise promotes the release of a wide array of signaling mediators from various metabolically active tissues and organs in the body. These exercise-induced signaling mediators could be the driving force behind some of the beneficial effects observed in brain with exercise. This review will aim to discuss potential exercise-induced signaling mediators with the capacity to influence various proteins involved in the formation of Aβ peptide production in the brain.
Keywords: amyloid precursor protein; brain; exercise; muscle; neuron.