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帕金森病的神经保护治疗:来自实验和遗传线索的现状和新方向。

Neuroprotective therapy in Parkinson's disease: current status and new directions from experimental and genetic clues.

机构信息

Committees on Neurobiology and Molecular Medicine, Departments of Neurology and Neurobiology, Pharmacology, & Physiology, The University of Chicago, USA.

出版信息

J Clin Neurol. 2005 Oct;1(2):107-20. doi: 10.3988/jcn.2005.1.2.107. Epub 2005 Oct 20.

DOI:10.3988/jcn.2005.1.2.107
PMID:20396458
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2854916/
Abstract

Despite successful treatment of Parkinson's disease (PD) with a wide variety of symptomatic therapy, the disease continues to progress and drug-resistance symptoms become the predominant factors producing the disability of PD patients. Neuroprotective therapies have been tested, but clinically effective drugs have not been found yet. New insights gained from studies of genetic forms of PD point to the common pathogenic mechanisms that have been suspected in sporadic forms of the disease and may provide new approaches for the future neuroprotective therapies.

摘要

尽管通过各种对症治疗成功地治疗了帕金森病 (PD),但该疾病仍在继续发展,并且耐药症状成为导致 PD 患者残疾的主要因素。已经测试了神经保护疗法,但尚未发现临床有效的药物。从 PD 的遗传形式研究中获得的新见解指向了在散发性疾病中已被怀疑的共同发病机制,并可能为未来的神经保护疗法提供新的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773e/2854916/521e5e6900b4/jcn-1-107-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773e/2854916/521e5e6900b4/jcn-1-107-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773e/2854916/521e5e6900b4/jcn-1-107-g001.jpg

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本文引用的文献

1
Disease progression continues in patients with advanced Parkinson's disease and effective subthalamic nucleus stimulation.在晚期帕金森病患者中,即使进行有效的丘脑底核刺激,疾病仍会继续进展。
J Neurol Neurosurg Psychiatry. 2005 Sep;76(9):1217-21. doi: 10.1136/jnnp.2004.057893.
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Genetics of Parkinson's disease.帕金森病的遗传学
Curr Opin Neurol. 2005 Aug;18(4):363-9. doi: 10.1097/01.wco.0000170951.08924.3d.
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Identification of risk and age-at-onset genes on chromosome 1p in Parkinson disease.帕金森病1号染色体上风险基因和发病年龄相关基因的鉴定
Am J Hum Genet. 2005 Aug;77(2):252-64. doi: 10.1086/432588. Epub 2005 Jun 28.
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Intake of vitamin E, vitamin C, and carotenoids and the risk of Parkinson's disease: a meta-analysis.维生素E、维生素C和类胡萝卜素的摄入与帕金森病风险:一项荟萃分析。
Lancet Neurol. 2005 Jun;4(6):362-5. doi: 10.1016/S1474-4422(05)70097-1.
5
High-dose creatine therapy for Huntington disease: a 2-year clinical and MRS study.高剂量肌酸疗法治疗亨廷顿病:一项为期2年的临床和磁共振波谱研究。
Neurology. 2005 May 10;64(9):1655-6. doi: 10.1212/01.WNL.0000160388.96242.77.
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Mutations in PTEN-induced putative kinase 1 associated with recessive parkinsonism have differential effects on protein stability.与隐性帕金森病相关的PTEN诱导的假定激酶1突变对蛋白质稳定性有不同影响。
Proc Natl Acad Sci U S A. 2005 Apr 19;102(16):5703-8. doi: 10.1073/pnas.0500617102. Epub 2005 Apr 11.
7
Age-dependent motor deficits and dopaminergic dysfunction in DJ-1 null mice.DJ-1基因敲除小鼠的年龄依赖性运动功能障碍和多巴胺能功能障碍
J Biol Chem. 2005 Jun 3;280(22):21418-26. doi: 10.1074/jbc.M413955200. Epub 2005 Mar 30.
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Physical activity and the risk of Parkinson disease.身体活动与帕金森病风险
Neurology. 2005 Feb 22;64(4):664-9. doi: 10.1212/01.WNL.0000151960.28687.93.
9
Nigrostriatal dopaminergic deficits and hypokinesia caused by inactivation of the familial Parkinsonism-linked gene DJ-1.家族性帕金森病相关基因DJ-1失活导致的黑质纹状体多巴胺能缺陷和运动迟缓。
Neuron. 2005 Feb 17;45(4):489-96. doi: 10.1016/j.neuron.2005.01.041.
10
Mixed lineage kinase-c-jun N-terminal kinase signaling pathway: a new therapeutic target in Parkinson's disease.混合谱系激酶 - c - jun N端激酶信号通路:帕金森病的新治疗靶点。
Mov Disord. 2005 Jun;20(6):653-64. doi: 10.1002/mds.20390.