期刊文献+

帕金森病运动并发症发生机制的研究进展 被引量:23

The potential mechanisms for motor complications of Parkinson's disease
下载PDF
导出
摘要 帕金森病是临床常见的中枢神经系统变性疾病,拟多巴胺类药物仍是其主要治疗手段。帕金森病患者长期接受多巴胺替代治疗后,可出现运动并发症,发生机制目前尚未完全阐明,而且对有些运动并发症仍缺乏有效的治疗方法,给帕金森病的治疗带来了困难和挑战。近年来,国内外学者对帕金森运动并发症的发生机制进行了广泛的研究,取得了显著进展,本文拟从左旋多巴药代动力学及药效学、神经生化学等角度阐述导致运动并发症的相关机制,以期为后续帕金森运动并发症的机制及治疗相关研究提供新视野。 Parkinson's disease (PD) is a common neurodegenerative disease. Dopaminergic replacement therapy is still considered as a major treatment for PD. However, long term dopaminergic replacement therapy for PD patients is frequently associated with the development of motor complications. To date, the mechanisms underlying motor complications have not been completely understood yet. Moreover, parts of motor complications are lack of therapeutic alternatives. All these characters make this disorder difficult and challenging to manage. Increasing number of researches have been proposed in recent years for elucidating the underlying mechanisms of levodopa related motor complications, resulting in much progression. For better understanding the management of motor complications, here we provide an overview of the current knowledge of the potential mechanisms, including the pharmacodynamic and pharmacokinetic mechanisms of levodopa and levodopa associated neurotransmitter systems.
作者 熊念 孙圣刚
出处 《中国现代神经疾病杂志》 CAS 2013年第8期656-662,共7页 Chinese Journal of Contemporary Neurology and Neurosurgery
基金 国家自然科学基金资助项目(项目编号:81200983)~~
关键词 帕金森病 运动障碍 左旋多巴 综述 Parkinson disease Movement disorders Levodopa Review
  • 相关文献

参考文献1

二级参考文献34

  • 1Drouot X, Oshino S, Jarraya B, et al. Functional recovery in a primate model of Parkinson's disease following motor cortex stimulation. Neuron, 2004, 44:769-778.
  • 2Benvenuti E, Cecchi F, Colombini A, et al. Extradural motor cortex stimulation as a method to treat advanced Parkinson's disease: new perspectives in geriatric medicine. Aging Clin Exp Res, 2006, 18:347-348.
  • 3Bjorklund LM, Sanchez-Pernaute R, Chung S, et al. Embryonic stem cells develop into functional dopaminergic neurons after transplantation in a Parkinson rat model. Proc Natl Acad Sci USA, 2002, 99:2344-2349.
  • 4Piccini P, Pavese N, Hagell P, et al. Factors affecting the clinical outcome after neural transplantation in Parkinson's disease. Brain, 2005, 128(Pt 12):2977-2986.
  • 5Wernig M, Zhao JP, Pruszak J, et al. Neurons derived from reprogrammed fibroblasts functionally integrate into the fetal brain and improve symptoms of rats with Parkinson's disease. Proc Natl Acad Sci USA, 2008, 105:5856-5861.
  • 6Kaplitt MG, Feigin A, Tang C, et al. Safety and tolerability of gene therapy with an adeno-associated virus (AAV) borne GAD gene for Parkinson's disease: an open label, phase Ⅰ trial. Lancet, 2007, 369:2097-2105.
  • 7Volz TJ, Farnsworth SJ, Rowley SD, et al. Age- dependent differences in dopamine transporter and vesicular monoautine transporter 2 function and their implications for methamphetamine neurotoxicity. Synapse, 2009, 63:147-151.
  • 8Youdim MB, Bakhle YS. Monoamine oxidase: isoforms and inhibitors in Parkinson's disease and depressive illness. Br J Pharmacol, 2006, 147 Suppl 1:287-296.
  • 9Morelli M, Carta AR, Jenner P. Adenosine A2A receptors and Parkinson's disease. Handb Exp Pharmacol, 2009, (193):589- 615.
  • 10Li J, Zhu M, Rajamani S, et al. Rifampicin inhibits alpha- synuclein fibrillation and disaggregates fibrils. Chem Biol, 2004, 11:1513-1521.

共引文献86

同被引文献219

引证文献23

二级引证文献175

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部