This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

William J. Freed, PhD
National Institute of Mental Health St Elizabeth's Hospital, 1 WAW Bldg Washington, DC 20032

Arch Neurol. 1984;41(11):1129-1130.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—Roach and Carlin¹ recently described a mentally retarded patient with severe seizures that were reduced by N,N-dimethylglycine. Lest potential therapeutic properties of N,N-dimethylglycine be too rapidly dismissed because of possible in vitro toxicity or because the compound has been promoted as a "health food",² I would like to point out some corroborative data. In fact, further consideration of clinical trials of N,N-dimethylglycine, and the related compound N,N,N,-trimethylglycine (betaine), for epilepsy has a sound scientific basis.

N,N-Dimethylglycine is formed from betaine in the metabolism of homocysteine to methionine.³ Betaine is the methyl donor only for the form of this reaction that occurs outside of the CNS.^4,5N,N-Dimethylglycine is thus formed from betaine by the removal of one methyl group. The involvement of betaine and N,N-dimethylglycine in homocysteine methylation is their only recognized biologic role.^3,6

Homocysteine can . . . [Full Text PDF of this Article]

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?