The cause of idiopathic Parkinson’s disease (IPD) is unknown, but reduced activity of complex I of the electron-transport chain has been implicated in the pathogenesis of IPD. Hyperhomocysteinemia is a well-established risk factor for cardiovascular and cerebrovascular diseases. However, recent evidence suggests that changes in the metabolic fate of homocysteine, leading to hyperhomocysteinemia, may also play a role in the pathophysiology of IPD.

Age and sex-matched 41 drug-naive IPD patients (16 men and 25 women) and 161 healthy controls (66 men and 95 women) were included in this study. Their fasting plasma homocystein and folate level, and the genotypes of methylenetetrahydrofolate reductase (MTHFR) were analyzed.

The plasma level of homocysteine was higher in untreated IPD patients (12.0±2.9 μmol/L) compared to the controls (9.0±2.6 μmol/L) (p =0.001). The frequencies of MTHFR C677T genotypes were not different between patients (CC:CT:TT=7:23:11) and controls (CC:CT:TT=27:86:48) (p =0.930). The adjusted odds ratio of homocysteine was remarkable (adjusted OR=1.149, 95% confidential interval=1.66–2.28, p =0.004).

IPD patients have higher plasma homocysteine level than healthy controls but MTHFR C667T genotype was not related to the homocysteine level. It can be suggested that increased plasma homocysteine level may contribute to the pathogenesis of IPD.