Department of Anatomy and Neuroscience, University College Cork, Cork, Ireland.
Department of Anatomy and Neuroscience, University College Cork, Cork, Ireland; APC Microbiome Institute, University College Cork, Cork, Ireland.
Neurobiol Aging. 2018 May;65:60-68. doi: 10.1016/j.neurobiolaging.2018.01.011. Epub 2018 Feb 2.
Parkinson's disease (PD) is no longer primarily classified as a motor disorder due to increasing recognition of the impact on patients of several nonmotor PD symptoms, including cognitive dysfunction. These nonmotor symptoms are highly prevalent and greatly affect the quality of life of patients with PD, and so, therapeutic interventions to alleviate these symptoms are urgently needed. The aim of this study was to investigate the potential neuroprotective effects of voluntary running on cognitive dysfunction in an adeno-associated virus-α-synuclein rat model of PD. Bilateral intranigral administration of adeno-associated virus-α-synuclein was found to induce motor dysfunction and a significant loss of nigral dopaminergic neurons, neither of which were rescued by voluntary running. Overexpression of α-synuclein also resulted in significant impairment on hippocampal neurogenesis-dependent pattern separation, a cognitive task; this was rescued by voluntary running. This was substantiated by an effect of running on neurogenesis levels in the dorsal dentate gyrus, suggesting that the functional effects of running on pattern separation were mediated via increased neurogenesis.
帕金森病（PD）不再主要被归类为运动障碍，因为人们越来越认识到几种非运动性 PD 症状对患者的影响，包括认知功能障碍。这些非运动症状非常普遍，极大地影响了 PD 患者的生活质量，因此，迫切需要治疗干预来减轻这些症状。本研究旨在探讨在 PD 的腺相关病毒-α-突触核蛋白大鼠模型中，自愿跑步对认知功能障碍的潜在神经保护作用。双侧纹状体注射腺相关病毒-α-突触核蛋白会导致运动功能障碍和黑质多巴胺能神经元的显著丧失，而自愿跑步并不能挽救这些损伤。α-突触核蛋白的过度表达也会导致海马神经发生依赖性模式分离（一种认知任务）的显著损伤，而自愿跑步可以挽救这种损伤。这一结果得到了跑步对背齿状回神经发生水平的影响的证实，表明跑步对模式分离的功能影响是通过增加神经发生介导的。
