The Systemic Effects of Exercise on the Systemic Effects of Alzheimer’s Disease

Abstract

Alzheimer’s disease (AD) is a progressive degenerative disorder and a leading cause of dementia in the elderly. The etiology of AD is multifactorial, including an increased oxidative state, deposition of amyloid plaques, and neurofibrillary tangles of the tau protein. The formation of amyloid plaques is considered one of the first signs of the illness, but only in the central nervous system (CNS). Interestingly, results indicate that AD is not just localized in the brain but is also found in organs distant from the brain, such as the cardiovascular system, gut microbiome, liver, testes, and kidney. These observations make AD a complex systemic disorder. Still, no effective medications have been found, but regular physical activity has been considered to have a positive impact on this challenging disease. While several articles have been published on the benefits of physical activity on AD development in the CNS, its peripheral effects have not been discussed in detail. The provocative question arising is the following: is it possible that the beneficial effects of regular exercise on AD are due to the systemic impact of training, rather than just the effects of exercise on the brain? If so, does this mean that the level of fitness of these peripheral organs can directly or indirectly influence the incidence or progress of AD? Therefore, the present paper aims to summarize the systemic effects of both regular exercise and AD and point out how common exercise-induced adaptation via peripheral organs can decrease the incidence of AD or attenuate the progress of AD.

Exercise combined with postbiotics treatment results in synergistic improvement of mitochondrial function in the brain of male transgenic mice for Alzheimer’s disease

“…LONP1 is responsible of removal of damaged proteins in the mitochondria, and because of excessive generation of ROS in this organelle this has a vital role in cell survival. AD is known to associated with increased oxidative stress (40,41), therefore the present novel observation, that exercise and postbiotic increase LONP-1 level and activity adds an important new mosaic to the better understanding of exercise and postbiotic treatments on AD.…”

Physical activity and the brain myelin content in humans

“…The only longitudinal study where the authors considered this relationship showed no relation between favorable changes in cardiorespiratory fitness evoked by intense aerobic exercise and myelin expansion (Mendez Colmenares et al, 2021). This finding is somewhat contradictory to the belief that exercise-induced changes in cardiovascular performance represent a key element in cognitive improvement (Aczel et al, 2022;Maleki et al, 2022;Renke et al, 2022).…”

Research trends and hotspots of exercise for Alzheimer’s disease: A bibliometric analysis

“…Therefore, removing the excessive accumulation of Aβ is an important train of thought in the treatment of AD. Exercise is considered an effective way to prevent and treat AD; such effectiveness may be related to the capability of exercise to participate in the clearance of the excessive accumulation of Aβ in the brain ( Radak et al, 2010 ; Aczel et al, 2022 ). Adlard et al (2005) published the study titled, “voluntary exercise decreases amyloid load in a transgenic model of Alzheimer’s disease,” in the Journal of Neuroscience, and it was possibly the earliest study on the clearance of Aβ by exercise.…”