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运动诱导的人类帕金森病神经可塑性:证据告诉了我们什么?

Exercise-induced neuroplasticity in human Parkinson's disease: What is the evidence telling us?

作者信息

Hirsch Mark A, Iyer Sanjay S, Sanjak Mohammed

机构信息

Carolinas Rehabilitation, Department of Physical Medicine and Rehabilitation, and Carolinas Neurosciences Institute, Carolinas Medical Center and HealthCare System, Charlotte, NC, USA.

Carolinas Rehabilitation, Department of Physical Medicine and Rehabilitation, and Carolinas Neurosciences Institute, Carolinas Medical Center and HealthCare System, Charlotte, NC, USA.

出版信息

Parkinsonism Relat Disord. 2016 Jan;22 Suppl 1:S78-81. doi: 10.1016/j.parkreldis.2015.09.030. Epub 2015 Sep 15.

Abstract

INTRODUCTION

While animal models of exercise and PD have pushed the field forward, few studies have addressed exercise-induced neuroplasticity in human PD.

METHOD

As a first step toward promoting greater international collaboration on exercise-induced neuroplasticity in human PD, we present data on 8 human PD studies (published between 2008 and 2015) with 144 adults with PD of varying disease severity (Hoehn and Yahr stage 1 to stage 3), using various experimental (e.g., randomized controlled trial) and quasi-experimental designs on the effects of cognitive and physical activity on brain structure or function in PD. We focus on plasticity mechanisms of intervention-induced increases in maximal corticomotor excitability, exercise-induced changes in voxel-based gray matter volume changes and increases in exercise-induced serum levels of brain derived neurotrophic factor (BDNF). Finally, we provide a future perspective for promoting international, collaborative research on exercise-induced neuroplasticity in human PD.

CONCLUSION

An emerging body of evidence suggests exercise triggers several plasticity related events in the human PD brain including corticomotor excitation, increases and decreases in gray matter volume and changes in BDNF levels.

摘要

引言

虽然运动和帕金森病的动物模型推动了该领域的发展,但很少有研究探讨运动诱导的人类帕金森病神经可塑性。

方法

作为促进人类帕金森病运动诱导神经可塑性方面更大国际合作的第一步,我们展示了8项关于人类帕金森病研究(2008年至2015年间发表)的数据,这些研究涉及144名疾病严重程度不同(霍恩和雅尔分期1至3期)的成年帕金森病患者,采用了各种实验性(如随机对照试验)和准实验设计,研究认知和身体活动对帕金森病患者脑结构或功能的影响。我们关注干预诱导的最大皮质运动兴奋性增加、运动诱导的基于体素的灰质体积变化以及运动诱导的血清脑源性神经营养因子(BDNF)水平升高的可塑性机制。最后,我们为促进人类帕金森病运动诱导神经可塑性的国际合作研究提供了未来展望。

结论

越来越多的证据表明,运动在人类帕金森病大脑中引发了几个与可塑性相关的事件,包括皮质运动兴奋、灰质体积的增加和减少以及BDNF水平的变化。

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