Physical exercise alleviates debilities of normal aging and Alzheimer's disease.
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.
Archer
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Department of Psychology, University of Gothenburg, Gothenburg, Sweden. Trevor.archer@psy.gu.se
D000375:Aging / Q000502:physiology*; D000544:Alzheimer Disease / Q000534:rehabilitation*; D000818:Animals; D015444:Exercise / Q000502:physiology*; D006801:Humans; D055495:Neurogenesis / Q000502:physiology; D010805:Physical Conditioning, Animal; D010809:Physical Fitness / Q000502:physiology*