期刊文献+

帕金森病内科治疗新策略 被引量:3

New strategies in treatment of parkinson's disease
下载PDF
导出
摘要 目前左旋多巴仍是治疗帕金森病的最有效药物,但所有的治疗措施仍停留在对症治疗阶段,并且长期应用左旋多巴会产生难以纠正的症状波动及异动症。针对帕金森病发病机制的研究热点,多种抗氧化应激、延缓细胞凋亡、改善线粒体功能及持续性多巴胺受体刺激的药物逐渐被应用于对帕金森病的治疗,这些药物有望延缓疾病进程,更好的改善临床症状。 Although levedopa remains the most effective drug for Parkinson's disease, there are some limitations of current PD therpy. For example, no drug is currently available to slow down or stop PD progression and current drug therapy is limited to symptomatic control of the motor symptoms of PD, most importantly, levedopa-induced motor fluctuation and dyskinesia are difficult to manage, so many new drugs are tested to interrupt the chains of pathogenesis of PD. Antioxidant, mitochondrial metabolism, slowing apoptosis drugs and continuous dopamigergic stimulation are tested with potential efficacyta limited slow down the development of PD and control symptoms without many complications.
作者 樊文辉 陈彪
出处 《基础医学与临床》 CSCD 北大核心 2005年第8期703-706,共4页 Basic and Clinical Medicine
基金 国家科技攻关计划(2004BA702B02) 国家重点基础研究发展计划(G2000057005)
关键词 神经保护 氧化应激 凋亡 治疗 neuroprotection oxidative stress apoptosis treatment
  • 相关文献

参考文献16

  • 1Przedborski S, Tieu K, Pefier C, et al. MPTP as a mitochondrial neurotoxie model of Parkinson's disease [J]. J Bioenergetics Biomembranes, 2004, 30(4) : 375 - 379.
  • 2Shimoda-Matsubayashi S, Hattori T, Matsumine H, et al. Mn SOD activity and protein in a patient with chromosome 6-linked autosomal recessive parkinsonism in comparison with Parkinson's disease and control [J]. Neurology, 1997, 49: 1257- 1262.
  • 3Shults CW, Haas RH, Passow D, et al. Coenzyme Q10 levels correlate with the activities of complex I and II/III in mitochondrial from Parkinsonian and nonparkinsonian subjects [J].Annual Neurol, 1997, 42(8) : 261 - 264.
  • 4Shults CW, Flint BM, Foutaine D, et al. Absorption, tolerability, and effects on mitochondrial activity of oral coenzyme Q10 in pakinsonian patients [J]. Neurology, 1998, 50(3) :793 - 795.
  • 5Hartmann A, Michel P, Twader JD, et al. Is BAX a mitochondrial mediator in apoptotic death of a dopaminergic neurons in Parkinson's disease? [J]. J Neurology, 2001, 76(6) : 1785 -1793.
  • 6Ziv I, Often D, Havid R, et al. The proto-oncogene Bcl-2 inhibits cellular toxicity of dopamine: possible implications for Parkinson's disease [J]. Apoptosis, 1997, 2(2): 149-155.
  • 7Kanthasamy AG, Kitazama MA, Kual SA, et al. Proteolytic activation of proapoptotic kinase PKC [ delta ] is regulated by overexpression of Bcl-2: implications for oxidative stress and environmental factors in Parkinson's disease [J]. Annals New York Academy Sciences, 2003, 1010: 683- 686.
  • 8Boll JB, Ceist MA, Schierle GS, et al. Improvement of embryonic dopaminergic neuron survival in culture and after grafting into the striatum of hemiparkinsonian rats by CEP-1347 [J]. J Neurochemistry, 2004, 88(3): 698-701.
  • 9Kitamura Y, Taniguchi T, Shimohama S, et al. Neuroprotectire mechanisms of antiparkinsonian dopamine Dz-receptor subfamily agonist [J]. Neurochemical Research, 2003, 28 (7) :1035 - 1040.
  • 10Gu M, Irvan M, Cooper JM, et al. Pramipexole protects against apoptotic cell death by non-dopaminergic mechanisms[J]. J Neurochemistry, 2004, 91(5) : 1075 - 1081.

同被引文献35

引证文献3

二级引证文献17

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