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作 者:房国梁[1] 王淑凡 杜晴丽 FANG Guoliang;WANG Shufan;DU Qingli(China Institute of Sport Science,Beijing 100061,China)
机构地区:[1]国家体育总局体育科学研究所,北京100061
出 处:《体育科学》2024年第9期71-80,共10页China Sport Science
基 金:国家体育总局体育科学研究所基本科研业务费资助项目(基本24-41);国家自然科学基金项目(31801004)。
摘 要:通过梳理钙稳态在运动改善阿尔茨海默症(Alzheimer’s disease,AD)中的作用及其机制的相关研究,发现钙稳态失衡与AD的发生发展密切相关,涉及β−(β-amyloid protein,Aβ)沉积、Tau蛋白异常磷酸化、线粒体功能障碍、自噬异常和神经炎症等多个方面。运动可调节机体钙稳态,具体表现为调节钙离子通道功能、促进肌浆网中钙离子释放和再摄取以及提高线粒体钙摄取等。运动通过调节钙稳态减少Aβ沉积、降低Tau蛋白磷酸化水平、改善线粒体功能障碍、改善自噬异常以及抑制神经炎症等,进而改善AD。未来需进一步探究运动调节钙稳态的分子机制,确定不同类型运动对不同人群的影响,并研究运动与其他干预手段的协同作用,为AD的预防和治疗提供新的思路和方法。This study reviewed the research progress in understanding the role and mechanism of calcium homeostasis in exercise improving Alzheimer’s disease(AD).It is found that calcium homeostasis imbalance is closely related to the occurrence and development of AD,which including multiple aspects such asβ-amyloid protein(Aβ)deposition,abnormal phosphorylation of Tau protein,mitochondrial dysfunction,autophagy abnormality,and neuroinflammation.Exercise can regulate calcium homeostasis in body,specifically manifested as regulating the function of calcium ion channels,promoting the release and reuptake of calcium ions in the sarcoplasmic reticulum,and increasing mitochondrial calcium uptake.By regulating calcium homeostasis,exercise reduces Aβdeposition,and the phosphorylation level of Tau protein,improves mitochondrial dysfunction and autophagy abnormality,suppresses neuroinflammation,thereby improving AD.In the future,it is necessary to further explore the molecular mechanism of exercise in regulating calcium homeostasis,and determine the impact of different exercise on different populations.In addition,and study the synergistic effect of exercise and other intervention methods should also be investigated so as to provide new ideas and methods for the prevention and treatment of AD.
关 键 词:钙稳态 运动 阿尔茨海默症 β−淀粉样蛋白 TAU蛋白
分 类 号:G804.7[文化科学—运动人体科学]
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