Physical exercise alleviates debilities of normal aging and Alzheimer’s disease

Abstract

Both healthy aging and the pathologic incidence of disorders associated with aging involve an array of debilities. Physical exercise harnesses implicit and inherent biologic characteristics amenable to the putative interventional influences under clinical, institutional or laboratory conditions. The neurodegenerative and pathophysiologic progressions that constitute Alzheimer's disease (AD), amnestic mild cognitive impairment (aMCI), normal aging, and different animal models of AD have shown the existence of several putative mechanisms. A large variety of moderating factors have demonstrated that the ever-proliferating plethora of neurotrophic factors, neurogenesis as observed through generality of expression and neuronal arborization. The insistent efficacy of brain vascular angiogenesis may delay also the comorbid incidence of depressive disorders with dementia pathology. The pathogenesis of aging may be contained by selective treatments: these diverse conditions, linked to the basis of the aging concept, have been shown, to greater or lesser extents, to respond to a variety of scheduled applications of physical exercise. The range of reports that provide accounts of the mechanisms mediating the positive progressive response to exercise intervention is far-ranging; these studies indicate that subtle changes at molecular, neuronal, vascular and epigenetic levels may exert notable consequence at functional expression and, perhaps most essentially, offer convincing expectancy of significant benefits.

The Effects of Long-term Exercise on Cerebral Function and the Maintenance of Concentration in the Elderly

“…Many epidemiological studies, intervention trials, and animal experiments have demonstrated that memory dysfunction, which is the predominant symptom of dementia and Alzheimer's disease, can be prevented and reduced in aged subjects through physical exercise [20][21][22]. However, the effects of physical exercise on mental concentration in the elderly are still unclear.…”

“…Nevertheless, there has been little information available about the effect of physical exercise on the levels of mental concentration in elderly people, whereas many reports state that physical exercise can prevent and improve memory impairment in adult humans [20][21][22].…”

Aspects of Cognition/Health Failure by HIV-infected Individuals: Amelioration through Exercise

“…Cross-sectional studies have indicated that activity and active engagement in daily activities bolsters neurocognitive functioning [39]. As implied by Mattson [40] and others [41][42][43][44][45][46], HAND patients ought to benefit from the plethora of health advantages bestowed by regular physical exercise: accelerated brain-derived factor and other trophic factor production, enhanced synaptic (even axonal) plasticity, neurogenesis and neuron arborization, increased production of anti-inflammatory cytokines and other aspects of improved neuroimmune functioning, and marked dividends for cognitive performance and affective balance. Furthermore, exercise intervention was applied to fifteen HIV-infected individuals between 35 and 51 years-of-age, and improvements in hand strength, scapular force, and several quality-of-life domains, including environment, perception of quality-of-life and global health [47,48].…”

The effect of exercise intervention on cognitive performance in persons at risk of, or with, dementia: A systematic review and meta-analysis

“…Severe, selective cortical atrophy in regions of the brain such as the temporal, medial temporal, limbic, frontal, and prefrontal cortices is one of the hallmarks of neurodegenerative and age-related dementia [5,6].…”

“…The functional and cognitive attributes affected by the deterioration of these brain structures include learning, memory, attention, motivation, executive function, motor function, global cognition, and activities during daily living [5,7]. MCI, which is often a prelude to dementia [8,9], is also associated with disproportionate atrophy in the medial temporal and temporal cortices [6,7].…”