神经科学
疾病
痴呆
陶氏病
心理学
衰老的大脑
医学
神经学
神经发生
阿尔茨海默病
神经营养素
体育锻炼
认知
神经退行性变
病理
内科学
受体
标识
DOI:10.1111/j.1600-0404.2010.01412.x
摘要
Archer T. Physical exercise alleviates debilities of normal aging and Alzheimer's disease.Acta Neurol Scand: 2011: 123: 221–238.© 2010 John Wiley & Sons A/S. 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.
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