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Is This a Problem?

Arch Neurol. 2004;61:633-634.

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

An elevated plasma concentration of total homocysteine (tHcy) is a risk factor for cardiac disease, stroke, vascular dementia, Alzheimer disease, and depression.^1-2 This may reflect a toxic effect of elevated tHcy, perhaps by free radical formation or inhibition of particular enzymes, or, alternatively, elevated tHcy may be a marker of disrupted 1-carbon metabolism.³ As shown in Figure 1, methylation of multiple intracellular molecules, including nucleic acids and proteins, uses S-adenosylmethionine (SAM) as the donor, which is converted to S-adenosylhomocysteine (SAH), which is in equilibrium with homocysteine. The regeneration of methionine, the precursor of SAM, occurs in neurons exclusively via methionine synthase, which requires methyltetrahydrofolate and vitamin B₁₂. Additionally, vitamin B₆ deficiency results in tHcy elevation by preventing the conversion by cystathionine -synthase of homocysteine to cystathionine.

Figure appears in full text version. S-Adenosylmethionine (SAM) donates 1-carbon groups during reactions by enzymes, including catechol O-methyltransferase (COMT). S-Adenosyl homocysteine (SAH) is . . . [Full Text of this Article]

Padraig O'Suilleabhain, MD
Department of Neurology
University of Texas Southwestern Medical Center
5323 Harry Hines Blvd
Dallas, TX 75390-9036
(e-mail: Padraig.Osuilleabhain@UTSouthwestern.edu)

Ramon Diaz-Arrastia, MD, PhD
Dallas

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