Abstract
Physical activity has systemic effects on the body, affecting almost every organ. It is important not only for general health and wellbeing, but also in the prevention of diseases. The mechanisms behind the therapeutic effects of physical activity are not completely understood; however, studies indicate these benefits are not confined to simply managing energy balance and body weight. They also include systemic factors which are released into the circulation during exercise and which appear to underlie the myriad of benefits exercise can elicit. It was shown that along with a number of classical cytokines, active tissues also engage in inter-tissue communication via extracellular vesicles (EVs), specifically exosomes and other small EVs, which are able to deliver biomolecules to cells and alter their metabolism. Thus, EVs may play a role in the acute and systemic adaptations that take place during and after physical activity, and may be therapeutically useful in the treatment of a range of diseases, including metabolic disorders such as type 2 diabetes and obesity; and the focus of this review, neurological disorders such as Alzheimer’s disease.
Highlights
Physical activity has systemic effects on the body, impacting most organs, including the brain
It is already known that exercise can protect against age-related cognitive decline, Alzheimer’s disease (AD) and vascular dementia [4], with prospective studies indicating that higher levels of physical activity are associated with reduced risk of developing these conditions [5]
Physical activity and increased fitness levels are associated with maintenance or improvements to brain biology and function, reducing the risk of dementia and AD; a number of large epidemiological and prospective studies have shown that exercise reduces the risks of dementia and AD by 28% and
Summary
Physical activity has systemic effects on the body, impacting most organs, including the brain. That evidence, along with the lack of effective therapies targeting Aβ pathology, has led to a shift in focus onto alternative interventions fueled by a large number of epidemiological studies and long-term randomized controlled trials These studies suggest that multidisciplinary lifestyle interventions, including exercise, can improve or maintain cognitive function and reduce incidents of AD in patients at risk of developing the disease [49,50,51,52]. While sustained exposure to many pro-inflammatory cytokines impairs both degradation of Aβ fibrils via microglia and degradation of Aβ oligomers via protease degradation and paravenous clearance, recently, evidence has suggested some pro-inflammatory signaling pathways may provide benefits in a mouse model of AD [61] Therapies or interventions such as exercise which promote activation of these beneficial pro-inflammatory pathways may reduce AD pathology by improving degradation and clearance of Aβ, thereby reducing neuronal loss and so preventing cognitive impairment. The level of insulin within the CNS is inversely correlated to the severity of AD and neurodegeneration, suggesting that impairment within the insulin signaling pathway plays a role in the pathology of AD
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