The ACE deletion polymorphism is not associated with Parkinson's disease

The deletion allele (D allele) polymorphism in the angiotensin converting e nzyme (ACE) gene is associated with increased levels of the neuropeptide su bstance P in the basal ganglia and substantia nigra. A reduction of substan ce P levels in the brain occurs in Parkinson's disease (PD) and has been im plicated in the pathogenesis of the disease. We investigated the hypothesis that the D allele may be protective towards PD by examining the frequency of the ACE (I/D) polymorphism in 178 PD cases (male:female ratio = 1.4) and 192 controls (male:female ratio = 1.5). ACE (I/D) genotype was determined using polymerase chain reaction and 3% agarose gel electrophoresis. Unadjus ted chi-square analysis revealed no significant difference between genotype frequencies (chi(2) = 3.30, p > 0.10) or allele frequencies (chi(2) = 2.52 , p > 0.10) between patient and control groups, although PD patients were l ess likely to be homozygous (OR = 0.80, 95% CI = 0.49-1.29) or heterozygous (OR = 0.80, 95% CI = 0.59-1.06) for the D allele. A stepwise logistic regr ession analysis of the ACE deletion and risk factor data confirmed that the re was no significant association between the ACE deletion (D allele) polym orphism and PD (OR = 0.62, 95% CI = 0.35-1.10, p = 0.10). This study does n ot support the hypothesis that the D allele of the ACE gene confers a prote ctive effect with respect to PD.