G2019S and R1441G are common LRRK2 mutations in PD patients in this region. PARKIN mutations override clinical features in LRRK2-associated PD.

G196A polymorphism is not a risk factor for PD and does not seem to modify clinical features in PD patients studied here.

LETTER TO THE EDITORSJON 2937 mopathy affecting about 400 million people worldwide [8]. We have shown that transgenic overexpression of G6PD in the nigrostriatal system of mice confers protection against neurotoxin-induced parkinsonism [7]. A marked decrease of G6PD activity in erythrocytes of Indian PD patients has been reported [1], so it was of immediate clinical interest to definitively asses any relationship between G6PD and PD. To this end, we have performed a case control study with a large sample of mainly Caucasian ethnic background, and using independent methods to estimate G6PD activity in two different cell types.A total of 165 PD patients (98 men and 67 women; mean age 63.9 ± 10.7 years) and 218 control subjects (135 men and 83 women; mean age 61.9 ± 11.3 years) were included. The mean age at onset of PD was 56.2 ± 12.3 years with an average evolution time of 7.8 ± 6.4 years. The current study was approved by the local ethical committee and written consent was obtained from all patients and control individuals who participated in the study.Peripheral blood was extracted to isolate erythrocytes and lymphocytes. G6PD activity was determined by measuring the rate of NADPH production spectrophotometrically [3,4]. In red blood cells (RBCs) of control sample, G6PD activity was not associated with age