Neuroprotective Clinical Studies in Parkinson's Disease

帕金森病的神经保护临床研究

• 批准号: 7012685
• 负责人: MARK F LEW
• 金额: $ 3.25万
• 依托单位: UNIVERSITY OF SOUTHERN CALIFORNIA
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-09-15 至 2007-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7012685
• 关键词: Parkinson' s disease; chemoprevention; clinical research; clinical trials; cooperative study; exercise; human subject; human therapy evaluation; medical outreach /case finding; nervous system disorder therapy; neuropharmacology; neurophysiology; neuroprotectants; patient oriented research

DESCRIPTION (provided by applicant): This proposal is in response to RFA-NS-02-010 Parkinson's Disease Neuroprotective Clinical Trials: Clinical Center. Parkinson's disease is a progressive and debilitating neurodegenerative disorder affecting one-percent of the population over the age of 55 years. The primary pathological features of PD are the loss of nigrostriatal dopaminergic neurons and subsequent depletion of striatal dopamine. The cause of PD is currently unknown but both environmental and genetic factors may contribute to the etiology of the disease. Since PD is a progressive disease, pharmacological and/or non-pharmacological modalities may be developed to provide neuroprotection through either protecting/rescuing surviving neurons and slowing disease progression. The primary goal of this proposal is to identify and recruit patients and conduct clinical trials of neuroprotection in early stage PD. An alternative approach to slowing disease progression is by promoting neuroplasticity in surviving nigrostriatal neurons. One possible non-pharmacological intervention is the process of activity-dependent neuroplasticity that may be achieved through long-term exercise (such as treadmill training). The secondary goal of this proposal is to determine if long-term treadmill training attenuates disease progression in PD through activity dependent neuroplasticity.

描述（由申请人提供）：该建议是对RFA-NS-02-010帕金森氏病神经保护临床试验的响应：临床中心。 帕金森氏病是一种渐进的和令人衰弱的神经退行性疾病，影响了55岁以上人口的百分比。 PD的主要病理特征是骨纹状体多巴胺能神经元的丧失以及随后的纹状体多巴胺的耗竭。 PD的原因目前尚不清楚，但环境和遗传因素都可能导致该疾病的病因。由于PD是一种进行性疾病，因此可以通过保护/营救幸存的神经元并减缓疾病进展来开发药理学和/或非药理方式来提供神经保护作用。该提案的主要目标是识别和招募患者并在早期PD进行神经保护的临床试验。减缓疾病进展的另一种方法是促进植物性神经元中的神经可塑性。一种可能的非药物干预是通过长期运动（例如跑步机训练）实现活动依赖性神经塑性的过程。该提案的次要目标是确定长期的跑步机训练是否通过依赖于活动的神经可塑性减轻了PD的疾病进展。