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Hyperhomocysteinemia and Neurologic Disorders: a Review

Journal of Clinical Neurology 2014³â 10±Ç 4È£ p.281 ~ 288
Ansari Ramin, Mahta Ali, Mallack Eric, Luo Jin Jun,
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 ( Ansari Ramin ) 
Temple University School of Medicine Department of Neurology

 ( Mahta Ali ) 
Temple University School of Medicine Department of Neurology
 ( Mallack Eric ) 
Weill Cornell Medical Center New York Presbyterian Hospital Department of Pediatrics
 ( Luo Jin Jun ) 
Temple University School of Medicine Department of Neurology

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.

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hyperhomocysteinemia; neurologic disorders; pregnancy

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