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余锋, 徐波, 何标, 张宪亮, 季浏. 运动缓解阿尔茨海默症与改善认知功能的生物学机制[J]. 上海体育学院学报 , 2017, 41(1): 25-31. DOI: 10.16082/j.cnki.issn.1001-4578.2017.05
引用本文: 余锋, 徐波, 何标, 张宪亮, 季浏. 运动缓解阿尔茨海默症与改善认知功能的生物学机制[J]. 上海体育学院学报 , 2017, 41(1): 25-31. DOI: 10.16082/j.cnki.issn.1001-4578.2017.05
YU Feng, XU Bo, HE Biao, ZHANG Xianliang, JI Liu. Biological Mechanism of Exercise Remitting Alzheimer's Disease and Ameliorating Recognition[J]. Journal of Shanghai University of Sport, 2017, 41(1): 25-31. DOI: 10.16082/j.cnki.issn.1001-4578.2017.05
Citation: YU Feng, XU Bo, HE Biao, ZHANG Xianliang, JI Liu. Biological Mechanism of Exercise Remitting Alzheimer's Disease and Ameliorating Recognition[J]. Journal of Shanghai University of Sport, 2017, 41(1): 25-31. DOI: 10.16082/j.cnki.issn.1001-4578.2017.05

运动缓解阿尔茨海默症与改善认知功能的生物学机制

Biological Mechanism of Exercise Remitting Alzheimer's Disease and Ameliorating Recognition

  • 摘要: 阿尔茨海默症(AD)是发生于老年期的神经系统退行性疾病,是导致老年性痴呆的最主要风险因素,目前还未发现能有效预防和治疗AD的策略。研究证实,运动能促进认知功能障碍患者以及实验动物学习记忆能力的提高。运动的优越性已得到AD动物实验的验证,运动可通过抑制脑内β-淀粉样蛋白的沉积和tau蛋白的过度磷酸化,改善AD的表观遗传学病理,促进脑源性神经营养因子等神经再生以及突触可塑性相关生长因子的表达,进而促进AD实验动物海马功能的恢复;运动还可抵御神经细胞线粒体和神经系统免疫功能障碍所致的衰老和AD的发病,缓解认知功能的衰退。

     

    Abstract: Alzheimer's disease (AD) is a neurodegenerative disease that occurs in senescence, which could be the main risk factor to lead to senile dementia. Currently, there is no effective strategy in the prevention and treatment of AD. Numerous studies have confirmed that exercise can promote learning and memory, including the patients with cognitive dysfunction or animals. The mechanisms underlying these benefits have been explored using animal models of AD. Accumulating studies show that exercise reinstates the testing animal hippocampal's function by inhibiting the deposition of Aβ and tau hyperphosphorylation, ameliorating the epigenetics mechanism of AD, and enhancing the expression of brain-derived neurotrophic factor (BDNF) and other growth factors that promote neurogenesis and synaptic plasticity. In addition, researchers have found that exercise may counteract aged or AD-associated declines in mitochondrial and immune system function.

     

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