Exercise is beneficial at every age, but most people do not undertake enough physical activity. In a sedentary world, structured exercise programs look like a decent therapy, because that exercise corrects a harmful deficiency in the operation of metabolism. Thus the studies showing a reduction in mortality resulting from exercise as an intervention in older individuals. Exercise improves mitochondrial function, amongst other changes, and these changes should be expected to modestly slow the progression of many age-related diseases.
Neurons are highly specialized post-mitotic cells that are inherently dependent on mitochondria due to their higher bioenergetic demand. Mitochondrial dysfunction is closely associated with a variety of aging-related neurological disorders, such as Alzheimer's disease (AD), and the accumulation of dysfunctional and superfluous mitochondria has been reported as an early stage that significantly facilitates the progression of AD. Mitochondrial damage causes bioenergetic deficiency, intracellular calcium imbalance, and oxidative stress, thereby aggravating β-amyloid (Aβ) accumulation and Tau hyperphosphorylation, and further leading to cognitive decline and memory loss.
Although there is an intricate parallel relationship between mitochondrial dysfunction and AD, their triggering factors, such as Aβ aggregation and hyperphosphorylated Tau protein, are still unclear. Moreover, many studies have confirmed abnormal mitochondrial biosynthesis, dynamics, and functions will present once the mitochondrial quality control is impaired, thus leading to aggravated AD pathological changes. Accumulating evidence shows beneficial effects of appropriate exercise on improved mitophagy and mitochondrial function to promote mitochondrial plasticity, reduce oxidative stress, enhance cognitive capacity and reduce the risks of cognitive impairment and dementia in later life. Therefore, stimulating mitophagy and optimizing mitochondrial function through exercise may forestall the neurodegenerative process of AD.