García-Mesa Yoelvis, Colie Sandra, Corpas Rubén, Cristòfol Rosa, Comellas Francesc, Nebreda Angel R, Giménez-Llort Lydia, Sanfeliu Coral
Institut d'Investigacions Biomèdiques de Barcelona - CSIC, Spain. Present address: Department of Molecular Biology and Microbiology, School of Medicine, Case Western Reserve University, Cleveland, Ohio.
Signalling and Cell Cycle Laboratory, Institute for Research in Biomedicine, Barcelona, Spain.
J Gerontol A Biol Sci Med Sci. 2016 Jan;71(1):40-9. doi: 10.1093/gerona/glv005. Epub 2015 Feb 26.
Physical exercise is suggested for preventing or delaying senescence and Alzheimer's disease (AD). We have examined its therapeutic value in the advanced stage of AD-like pathology in 3xTg-AD female mice through voluntary wheel running from 12 to 15 months of age. Mice submitted to exercise showed improved body fitness, immunorejuvenation, improvement of behavior and cognition, and reduced amyloid and tau pathology. Brain tissue analysis of aged 3xTg-AD mice showed high levels of oxidative damage. However, this damage was decreased by physical exercise through regulation of redox homeostasis. Network analyses showed that oxidative stress was a central event, which correlated with AD-like pathology and the AD-related behaviors of anxiety, apathy, and cognitive loss. This study corroborates the importance of redox mechanisms in the neuroprotective effect of physical exercise, and supports the theory of the crucial role of oxidative stress in the switch from normal brain aging to pathological aging and AD.
建议进行体育锻炼以预防或延缓衰老及阿尔茨海默病（AD）。我们通过在12至15月龄的3xTg-AD雌性小鼠中进行自愿转轮运动，研究了其在AD样病理晚期的治疗价值。进行运动的小鼠身体适应性得到改善，免疫功能恢复，行为和认知能力提高，淀粉样蛋白和tau病理减少。对老年3xTg-AD小鼠的脑组织分析显示氧化损伤水平较高。然而，通过调节氧化还原稳态，体育锻炼降低了这种损伤。网络分析表明氧化应激是一个核心事件，它与AD样病理以及焦虑、冷漠和认知丧失等AD相关行为相关。本研究证实了氧化还原机制在体育锻炼神经保护作用中的重要性，并支持氧化应激在从正常脑衰老向病理性衰老和AD转变中起关键作用的理论。
