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To the Editor:
We read with interest the article by Miller et al. describing the effect of l-dopa on plasma homocysteine in Parkinson disease (PD).1 We welcome the attention that this important metabolic phenomenon now receives, as we think that l-dopa–induced hyperhomocystenemia in PD is indicative of a broader metabolic alteration of the trans- methyl pathway with potential clinical consequences that extend beyond vascular disease and dementia.
As reported by the authors,1 the increase in homocysteine is due to l-dopa O- methylation, a reaction catalyzed by catechol-O-methyltransferase (COMT). This reaction consumes the methyl donor S-adenosylmethionine, the principal methyl-group donor in the brain, and leads to increased production of (demethylated) S- adenosylhomocysteine, and, ultimately, homocysteine. Increased O-methylation, however, cannot only lead to hyperhomocystenemia, but can also cause a depletion of S- adenosylmethionine, inducing a state of relative hypomethylation. In addition to COMT- dependent O-methylation of catecholamines, S-adenosylmethionine is the methylating agent in vital metabolic reactions, including the synthesis of phosphatidylcholine and creatine, the methylation of phospholipids and of proteins, including N- and carboxyl- methylation of proteins, essential for the proper function of receptors configuration and permeability of ion channels.2 Of immediate clinical relevance is the fact that S- adenosylmethionine depletion has been associated with depression, common in patients with Parkinson …
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