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本文引用的文献

1
Pathogenesis-targeted, disease-modifying therapies in Parkinson disease.帕金森病中针对发病机制的疾病修饰疗法。
Neurotherapeutics. 2014 Jan;11(1):6-23. doi: 10.1007/s13311-013-0218-1.
2
Plasma homocysteine levels in patients with multiple sclerosis in the Greek population.希腊人群多发性硬化症患者的血浆同型半胱氨酸水平。
J Chin Med Assoc. 2013 Nov;76(11):611-4. doi: 10.1016/j.jcma.2013.07.002. Epub 2013 Aug 8.
3
Folic acid supplementation does not reduce intracellular homocysteine, and may disturb intracellular one-carbon metabolism.叶酸补充并不能降低细胞内同型半胱氨酸水平,反而可能扰乱细胞内一碳代谢。
Clin Chem Lab Med. 2013 Aug;51(8):1643-50. doi: 10.1515/cclm-2012-0694.
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Peripheral neuropathy in Parkinson's disease: levodopa exposure and implications for duodenal delivery.帕金森病的周围神经病变:左旋多巴的暴露及其对十二指肠给药的影响。
Parkinsonism Relat Disord. 2013 May;19(5):501-7 ; discussion 501. doi: 10.1016/j.parkreldis.2013.02.006. Epub 2013 Feb 27.
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Elevated homocysteine levels in levodopa-treated idiopathic Parkinson's disease: a meta-analysis.左旋多巴治疗的特发性帕金森病患者同型半胱氨酸水平升高:一项荟萃分析。
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The genetics of Parkinson's disease: progress and therapeutic implications.帕金森病的遗传学:进展与治疗意义。
Mov Disord. 2013 Jan;28(1):14-23. doi: 10.1002/mds.25249.
7
Conversion from mild cognitive impairment to dementia: influence of folic acid and vitamin B12 use in the VITA cohort.从轻度认知障碍到痴呆的转化:叶酸和维生素 B12 使用对 VITA 队列的影响。
J Nutr Health Aging. 2012 Aug;16(8):687-94. doi: 10.1007/s12603-012-0051-y.
8
Relationship of cognitive function with B vitamin status, homocysteine, and tissue factor pathway inhibitor in cognitively impaired elderly: a cross-sectional survey.认知功能与维生素 B 状态、同型半胱氨酸和组织因子途径抑制剂在认知障碍老年人中的关系:一项横断面调查。
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10
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高同型半胱氨酸血症与神经障碍疾病:综述

Hyperhomocysteinemia and neurologic disorders: a review.

机构信息

Department of Neurology, Temple University School of Medicine, Philadelphia, PA, USA.

Department of Pediatrics, Weill Cornell Medical Center-New York Presbyterian Hospital, New York, NY, USA.

出版信息

J Clin Neurol. 2014 Oct;10(4):281-8. doi: 10.3988/jcn.2014.10.4.281. Epub 2014 Oct 6.

DOI:10.3988/jcn.2014.10.4.281
PMID:25324876
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4198708/
Abstract

Homocysteine (Hcy) is a sulfur-containing amino acid that is generated during methionine metabolism. It has a physiologic role in DNA metabolism via methylation, a process governed by the presentation of folate, and vitamins B6 and B12. Physiologic Hcy levels are determined primarily by dietary intake and vitamin status. Elevated plasma levels of Hcy (eHcy) can be caused by deficiency of either vitamin B12 or folate, or a combination thereof. Certain genetic factors also cause eHcy, such as C667T substitution of the gene encoding methylenetetrahydrofolate reductase. eHcy has been observed in several medical conditions, such as cardiovascular disorders, atherosclerosis, myocardial infarction, stroke, minimal cognitive impairment, dementia, Parkinson's disease, multiple sclerosis, epilepsy, and eclampsia. There is evidence from laboratory and clinical studies that Hcy, and especially eHcy, exerts direct toxic effects on both the vascular and nervous systems. This article provides a review of the current literature on the possible roles of eHcy relevant to various neurologic disorders.

摘要

同型半胱氨酸(Hcy)是一种含硫氨基酸,在蛋氨酸代谢过程中产生。它在 DNA 代谢的甲基化过程中具有生理作用,该过程受叶酸、维生素 B6 和 B12 的呈现调控。生理 Hcy 水平主要由饮食摄入和维生素状况决定。血浆 Hcy 水平升高(eHcy)可由维生素 B12 或叶酸缺乏或两者共同引起。某些遗传因素也会导致 eHcy,例如编码亚甲基四氢叶酸还原酶的基因 C667T 取代。在几种医学病症中都观察到了 eHcy,例如心血管疾病、动脉粥样硬化、心肌梗死、中风、轻度认知障碍、痴呆、帕金森病、多发性硬化症、癫痫和子痫。实验室和临床研究的证据表明,Hcy,尤其是 eHcy,对血管和神经系统都有直接的毒性作用。本文综述了 eHcy 与各种神经紊乱相关的可能作用的现有文献。