and motor function . preserves

Oxidative damage has been suggested as a potential mechanism for both atherosclerosis and neurodegenerative disorders such as Parkinson's disease.' One report has noted a 2-5-fold increased risk of cardiovascular disease among patients with Parkinson's disease,2 suggesting that a common genetic variant may contribute to both diseases. One such candidate genetic factor, the ApoE-E4 allele, is found at a raised frequency in those with cardiovascular disease and Alzheimer's disease, but was recently shown not to be raised in patients with Parkinson's disease.3 Homocysteine is a pro-oxidant that acts via the copper catalysed, oxygen dependent, production of hydrogen peroxide. Moderately raised concentrations of the amino acid homocysteine (mild hyperhomocysteinaemia) confer a twofold to threefold risk of vascular disease. In a significant proportion of cases mild hyperhomocysteinaemia arises from the interaction of the homozygous thermolabile (tt) genotype of 5,10-methylenetetrahydrofolate reductase (MTHFR) with suboptimal folate and B12 nutrition.4 The tt genotype has also been directly associated with cardiovascular disease.5 We therefore determined the prevalence of the tt genotype in patients with Parkinson's dis-