Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Oct;10(4):281-8.
doi: 10.3988/jcn.2014.10.4.281. Epub 2014 Oct 6.

Hyperhomocysteinemia and neurologic disorders: a review

Affiliations
Review

Hyperhomocysteinemia and neurologic disorders: a review

Ramin Ansari et al. J Clin Neurol. 2014 Oct.

Erratum in

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.

Keywords: hyperhomocysteinemia; neurologic disorders; pregnancy.

PubMed Disclaimer

Conflict of interest statement

The authors have no financial conflicts of interest.

Similar articles

Cited by

References

    1. Maxwell SR. Coronary artery disease--free radical damage, antioxidant protection and the role of homocysteine. Basic Res Cardiol. 2000;95(Suppl 1):I65–I71. - PubMed
    1. Graham IM, O'Callaghan P. Vitamins, homocysteine and cardiovascular risk. Cardiovasc Drugs Ther. 2002;16:383–389. - PubMed
    1. Finkelstein JD. The metabolism of homocysteine: pathways and regulation. Eur J Pediatr. 1998;157(Suppl 2):S40–S44. - PubMed
    1. Selhub J. Homocysteine metabolism. Annu Rev Nutr. 1999;19:217–246. - PubMed
    1. Pietrzik K, Brönstrup A. Vitamins B12, B6 and folate as determinants of homocysteine concentration in the healthy population. Eur J Pediatr. 1998;157(Suppl 2):S135–S138. - PubMed