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The role of exercise in facilitating basal ganglia function in Parkinson's disease

机译:运动在促进帕金森病中基底神经节功能中的作用

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Epidemiologicaland clinical studies have suggested that exercise is beneficial for patients with Parkinson's disease (PD). Through research in normal (noninjured) animals, neuroscientists have begun to understand the mechanisms in the brain by which behavioral training and exercise facilitates improvement in motor behavior through modulation of neuronal function and structure, called experience-dependent neuroplasticity. Recent studies are beginning to reveal molecules and downstream signaling pathways that are regulated during exercise and motor learning in animal models of PD and that are important in driving protective and/or adaptive changes in neuronal connections of the basal ganglia and related circuitry. These molecules include the neurotransmitters dopamine and glutamate (and their respective receptors) as well as neurotrophic factors (brain-derived neurotrophic factor). In parallel, human exercise studies have been important in revealing 'proof of concept' including examining the types and parameters of exercise that are important for behavioral/ functional improvements and brain changes; the feasibility of incorporating and maintaining an exercise program in individuals with motor disability; and, importantly, the translation and investigation of exercise effects observed in animal studies to exercise effects on brain and behavior in individuals with PD. In this article we highlight findings from both animal and human exercise studies that provide insight into brain changes of the basal ganglia and its related circuitry and that support potentially key parameters of exercise that may lead to long-term benefit and disease modification in PD. In addition, we discuss the current and future impact on patient care and point out gaps in our knowledge where continuing research is needed. Elucidation of exercise parameters important in driving neuroplasticity, as well as the accompanying mechanisms that underlie experience-dependent neuroplasticity may also pr...
机译:流行病学和临床研究表明,运动对帕金森氏病(PD)患者有益。通过对正常(非受伤)动物的研究,神经科学家已经开始了解大脑中的机制,通过这种机制,行为训练和运动可通过调节神经元功能和结构来促进运动行为的改善,称为经验依赖型神经可塑性。最近的研究开始揭示分子和下游信号传导途径,这些分子和下游信号传导途径在PD动物模型的运动和运动学习过程中受到调节,并且在驱动基底神经节和相关电路的神经元连接的保护性和/或适应性变化方面很重要。这些分子包括神经递质多巴胺和谷氨酸(及其各自的受体)以及神经营养因子(脑源性神经营养因子)。同时,人类运动研究对于揭示“概念验证”也很重要,其中包括检查运动的类型和参数,这些行为对行为/功能的改善和脑部改变至关重要。在运动障碍者中纳入和维持锻炼计划的可行性;而且,重要的是,将动物研究中观察到的运动效果的翻译和研究,转化为运动对PD患者大脑和行为的影响。在本文中,我们将重点介绍动物和人类运动研究的发现,这些发现可洞悉基底神经节及其相关电路的大脑变化,并支持运动的潜在关键参数,这些参数可能会导致PD的长期获益和疾病改变。此外,我们讨论了当前和未来对患者护理的影响,并指出了需要继续研究的知识方面的差距。阐明在驱动神经可塑性中起重要作用的运动参数,以及依赖于经验依赖的神经可塑性的伴随机制也可能会引起...

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