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Homocysteine – A Marker for Vitamin Deficiency and a Risk Factor for Neurological Diseases Homocysteine (Hcy) is the demethylated product of methionine. This toxic amino acid can be removed by remethylation to methionine via methionine synthase, which utilises 5-methyl tetrahydrofolate as a methyl donor and methyl cobalamin as a co-factor. An alternative remethylation pathway for Hcy depends on betaine-Hcy-methyltransferase, which utilises betaine as a methyl donor. Another method of Hcy catabolism is via two vitamin-B6-dependent enzymes, cystathionine beta synthase and cystathioninase, to cysteine. The catabolism of Hcy in the brain depends mainly on its remethylation to methionine, utilising folate and methyl cobalamin. Because B vitamins (folate, vitamin B12, vitamin B6) are important co-factors for Hcy catabolism, an elevated concentration of Hcy can indicate B-vitamin deficiency.1 An important role of Hcy-methionine metabolism is to provide S-adenosylmethionine (SAM), the methyl donor for numerous biological reactions. SAM donates its methyl group to a methyl acceptor and is transformed to S-adenosylhomocysteine (SAH). SAH is hydrolysed to Hcy by SAH-hydrolase. The SAH-hydrolase reaction is reversible, but favours SAH formation in the presence of increased Hcy. Hcy metabolism in the brain is an important source of SAM.2 This methyl donor plays important roles in the formation and catabolism of neurotransmitters and phospholipids (phosphatidylcholine is the methylated product of phosphatidylethanolamine), DNA methylation and activation of several enzymes that have essential roles in the brain (e.g. protein phosphatase 2A [PP2A]). Elevated levels of Hcy can therefore cause damage to several key pathways in the central nervous system, either directly or by changing the methylation potential (SAM/SAH).

Evaluation of the Current Evidence on Hyperhomocysteinaemia in Neurological Diseases