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.