在levodopa诱导的动力障碍中神经可塑性:病理生理学和治疗点的概述
Francesco Bove1, Benedetta Angeloni2, Pasquale Sanginario2
1Neurology Unit, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy; Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy.
Progress in neurobiology
|December 1, 2023
概括
帕金森病患者由于大脑可塑性受损而发展出非自愿的运动 (勒沃多巴诱导的动力障碍). 神经调节技术有可能恢复正常的大脑功能并治疗这些运动障碍.
科学领域:
- 神经科学是一个神经科学.
- 运动障碍 运动障碍
- 神经可塑性 神经可塑性
背景情况:
- 莱沃多巴诱导的运动障碍 (LID) 是帕金森病 (PD) 的常见并发症.
- 皮层-基底质系统的异常可塑性是LID病理生理学的基础.
- 条纹体中的突触可塑性对于运动控制至关重要.
研究的目的:
- 审查PD和LID中神经可塑性损伤的证据.
- 通过准异常可塑性来探索治疗LID的神经调制策略.
主要方法:
- 对PD和LID进行实验模型和人体研究的审查.
- 分析突触可塑性 (LTP/LTD) 在PD进展中的作用.
- 对神经调节技术 (DBS,TMS,tDCS) 的检查.
主要成果:
- PD和LID与长期潜能受损 (LTP) 和长期抑郁症 (LTD) 相关.
- 改变的可塑性导致网络失调和非自愿的运动.
- 神经可塑性缺陷在深层大脑结构和运动皮层中都被观察到.
结论:
- 在皮层-基底质网络中神经可塑性受损是LID的核心.
- 神经调节疗法在患有LID的PD患者中恢复神经生理功能方面表现有前途.
- 向异常可塑性可能为运动障碍提供有效的治疗策略.
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