Previously our study has demonstrated that long-term treadmill exercise improved cognitive deficit in APP/PS1 transgenic mice of Alzheimer's disease (AD) paralleled by enhanced long-term potentiation (LTP). The present study was undertaken to further investigate whether the treadmill running could inhibit the progression of Alzheimer's disease (AD)-like neuropathology in hippocampus of the APP/PS1 mouse models of AD, and to define a potential molecular mechanism underlying the exercise-induced reduction in AD-like neuropathology. Five months of treadmill exercise resulted in a robust reduction in β-amyloid (Aβ) deposition and tau phosphorylation in the hippocampus of APP/PS1 mice. This was accompanied by a significant decrease in APP phosphorylation and PS1 expression. We also observed GSK3, rather than CDK5, was inhibited by treadmill exercise. These results indicate that treadmill exercise is sufficient to inhibit the progression of AD-like neuropathology in the hippocampus of APP/PS1 transgenic mouse model, and may mediate APP processing in favor of reduced Aβ deposition. In addition, we demonstrate that treadmill exercise attenuates AD-like neuropathology in AD transgenic mice via a GSK3 dependent signaling pathway.

译文

:先前的研究表明,长期的跑步机锻炼可改善阿尔茨海默氏病(AD)的APP / PS1转基因小鼠的认知功能障碍,同时增强长期增强能力(LTP)。进行本研究以进一步调查跑步机是否可以抑制AD / APP1小鼠AD模型海马中的阿尔茨海默氏病(AD)样神经病理的进展,并确定运动诱导的降低的潜在分子机制在AD样神经病理学中。五个月的跑步机运动导致APP / PS1小鼠海马中β淀粉样蛋白(Aβ)沉积和tau磷酸化的明显降低。这伴随着APP磷酸化和PS1表达的显着降低。我们还观察到跑步机锻炼会抑制GSK3,而不是CDK5。这些结果表明,跑步机运动足以抑制APP / PS1转基因小鼠模型海马中AD样神经病理的进展,并可能介导APP的处理,从而减少Aβ的沉积。此外,我们证明了跑步机运动通过依赖GSK3的信号通路减弱了AD转基因小鼠的AD样神经病理。

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