Plasma Homocysteine and L-DOPA Metabolism in Pa- tients with Parkinson Disease, Fabio Blandini,1 * Roberto

Homocysteine is formed by demethylation of methionine and is involved in transmethylation mechanisms. Hyper-homocysteinemia is associated with a wide range of clinical manifestations, mostly affecting the central ner-vous system (e.g., mental retardation, cerebral atrophy, and epileptic seizures) (1, 2). Hyperhomocysteinemia has also been associated with an increased risk for atheroscle-rotic and thrombotic vascular diseases (3–5). Although various mechanisms have been proposed, mostly involv-ing endothelial damage related to increased oxidative stress (6), the exact cellular and molecular bases for the adverse effects of homocysteine are still elusive. Alterations in transmethylation reactions that lead to hyperhomocysteinemia have been suggested in the patho-physiology of neurodegenerative disorders such a