Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, 9177948564, Iran.
Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Metab Brain Dis. 2019 Feb;34(1):21-37. doi: 10.1007/s11011-018-0343-y. Epub 2018 Nov 15.
Alzheimer's disease (AD) is a fastest growing neurodegenerative condition with no standard treatment. There are growing evidence about the beneficial effects of exercise in brain health promotion and slowing the cognitive decline. The aim of this study was to review the protective mechanisms of treadmill exercise in different models of rodent memory deficits. Online literature database, including PubMed-Medline, Scopus, Google scholar were searched from 2003 till 2017. Original article with English language were chosen according to following key words in the title: (exercise OR physical activity) AND (memory OR learning). Ninety studies were finally included in the qualitative synthesis. The results of these studies showed the protective effects of exercise on AD induced neurodegerative and neuroinflammatory process. Neuroperotective effects of exercise on the hippocampus seem to be increasing in immediate-early gene c-Fos expression in dentate gyrus; enhancing the Wnt3 expression and inhibiting glycogen synthase kinase-3β expression; increasing the 5-bro-mo-2'-deoxyridine-positive and doublecortin-positive cells (dentate gyrus); increasing the level of astrocytes glial fibrillary acidic protein and decrease in S100B protein, increasing in blood brain barrier integrity; prevention of oxidative stress injury, inducing morphological changes in astrocytes in the stratum radiatum of cornu ammonis 1(CA1) area; increase in cell proliferation and suppress apoptosis in dentate gyrus; increase in brain-derived neurotrophic factor and tropomyosin receptor kinase B expressions; enhancing the glycogen levels and normalizing the monocarboxylate transporter 2 expression.
阿尔茨海默病（AD）是一种增长最快的神经退行性疾病，目前尚无标准治疗方法。越来越多的证据表明，运动对大脑健康有促进作用，可以减缓认知能力下降。本研究旨在综述跑步机运动对不同啮齿动物记忆缺陷模型的保护机制。检索了 2003 年至 2017 年期间在线文献数据库，包括 PubMed-Medline、Scopus、Google Scholar。根据标题中的以下关键词（“运动”或“体力活动”和“记忆”或“学习”）选择具有英文语言的原始文章。最终有 90 项研究被纳入定性综合分析。这些研究的结果表明，运动对 AD 引起的神经退行性和神经炎症过程具有保护作用。运动对海马体的神经保护作用似乎表现为齿状回中即刻早期基因 c-Fos 表达增加；增强 Wnt3 表达，抑制糖原合酶激酶-3β表达；增加 5-溴-2'-脱氧尿苷阳性和双皮质素阳性细胞（齿状回）；增加星形胶质细胞神经丝酸性蛋白水平，减少 S100B 蛋白，增加血脑屏障完整性；预防氧化应激损伤，诱导 CA1 区放射层星形胶质细胞形态改变；增加细胞增殖，抑制齿状回细胞凋亡；增加脑源性神经营养因子和原肌球蛋白受体激酶 B 的表达；增加糖原水平，使单羧酸转运蛋白 2 表达正常化。
