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首页> 外文期刊>The European Journal of Neuroscience >Neuroprotective effects and mechanisms of exercise in a chronic mouse model of Parkinson's disease with moderate neurodegeneration.
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Neuroprotective effects and mechanisms of exercise in a chronic mouse model of Parkinson's disease with moderate neurodegeneration.

机译：在帕金森氏病伴中度神经变性的慢性小鼠模型中，神经保护作用和运动机制。

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摘要

The protective impact of exercise on neurodegenerative processes has not been confirmed, and the mechanisms underlying the benefit of exercise have not been determined in human Parkinson's disease or in chronic animal disease models. This research examined the long-term neurological, behavioral, and mechanistic consequences of endurance exercise in experimental chronic parkinsonism. We used a chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse model of Parkinson's disease with moderate neurodegeneration and examined the effects of treadmill exercise on movement and balance coordination, changes in dopamine neuron biomarkers, mitochondrial functions, and neurotrophic factor activities in the nigrostriatal system. The exercise results were compared with those of the control and sedentary chronic parkinsonian animals. After 18 weeks of exercise training in the chronic parkinsonian mice, we observed a significant deterrence in the loss of neuronal dopamine-producing cells and other functional indicators. The impaired movement and balance incoordination in the chronic parkinsonian mice were also markedly reduced following exercise. Mechanistic investigations revealed that the neuronal and behavioral recovery produced by exercise in the chronic parkinsonian mice was associated with an improved mitochondrial function and an increase in the brain region-specific levels of brain-derived and glial cell line-derived neurotrophic factors. Our findings indicate that exercise not only produces neuronal and mitochondrial protection, it also boosts nigrostriatal neurotrophic factor levels in the chronic parkinsonian mice with moderate neurodegeneration. Therefore, modifying lifestyle with increased exercise activity would be a non-pharmacological neuroprotective approach for averting neurodegenerative processes, as demonstrated in experimental chronic parkinsonism.
机译：运动对神经变性过程的保护作用尚未得到证实，运动益处的根本机制尚未在人帕金森氏病或慢性动物疾病模型中确定。这项研究检查了耐力运动在实验性慢性帕金森病中的长期神经，行为和机制后果。我们使用了慢性1-甲基-4-苯基-1,2,3,6-四氢吡啶诱发的帕金森氏病伴中度神经退行性病变的小鼠模型，并研究了跑步机对运动和平衡协调，多巴胺神经元生物标志物变化的影响，纹状体系统的线粒体功能和神经营养因子活性。将运动结果与对照和久坐的慢性帕金森病动物的运动结果进行比较。在慢性帕金森病小鼠中进行了18周的运动训练后，我们观察到神经元多巴胺产生细胞和其他功能指标的丧失具有显着的威慑力。运动后，慢性帕金森病小鼠的运动障碍和平衡不协调也明显减少。机理研究表明，在慢性帕金森病小鼠中运动产生的神经元和行为恢复与线粒体功能的改善以及脑源性和胶质细胞源性神经营养因子在脑区域特定水平的升高有关。我们的研究结果表明，运动不仅可以保护神经元和线粒体，还可以增强患有中度神经变性的慢性帕金森病小鼠的黑纹状体神经营养因子水平。因此，通过增加运动活动来改变生活方式将是避免神经退行性过程的一种非药理性神经保护方法，如实验性慢性帕金森病所证明的那样。

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