title: Association between angiotensin-converting enzyme and Alzheimer disease.
abstract: BACKGROUND
  Angiotensin-converting enzyme has been reported to show altered activity in patients with neurologic diseases. An insertion-deletion polymorphism in ACE has recently been linked to heart disease, cerebrovascular disease, and AD.
  
  
  OBJECTIVE
  To determine whether the angiotensin-converting enzyme (ACE) is associated with risk of Alzheimer disease (AD).
  
  
  METHODS
  We investigated the ACE polymorphism as a potential risk factor for AD in 151 patients with AD and 206 ethnically matched controls from Russia and in 236 patients with AD and 169 controls from North America by means of allele association methods and logistic regression.
  
  
  RESULTS
  None of the ACE genotypes was associated with increased susceptibility to AD in the total sample or in subsets stratified by apolipoprotein E gene (APOE) epsilon4 status. However, the D allele was more frequent among AD cases between ages 66 and 70 years compared with controls in both the Russian (P = .02) and North American (P = .001) datasets. In this age group, the effect of D (odds ratio, 11.2; 95% confidence interval, 2.9-44.0) appeared to be independent of and equal or greater in magnitude to the effect of APOE epsilon4 (odds ratio, 7.8; 95% confidence interval, 3.5-7.4).
  
  
  CONCLUSIONS
  Our results suggest that APOE and ACE genotypes may be independent risk factors for late-onset AD, but the ACE association needs to be confirmed in independent samples in which the time and extent of vascular cofactors can be assessed.
authors.affiliation: Department of Medicine (Genetics Program), Boston University School of Medicine, Mass, USA.
authors.forename: L A
authors.initials: LA
authors.lastname: Farrer
authors.forename: T
authors.initials: T
authors.lastname: Sherbatich
authors.forename: S A
authors.initials: SA
authors.lastname: Keryanov
authors.forename: G I
authors.initials: GI
authors.lastname: Korovaitseva
authors.forename: E A
authors.initials: EA
authors.lastname: Rogaeva
authors.forename: S
authors.initials: S
authors.lastname: Petruk
authors.forename: S
authors.initials: S
authors.lastname: Premkumar
authors.forename: Y
authors.initials: Y
authors.lastname: Moliaka
authors.forename: Y Q
authors.initials: YQ
authors.lastname: Song
authors.forename: Y
authors.initials: Y
authors.lastname: Pei
authors.forename: C
authors.initials: C
authors.lastname: Sato
authors.forename: N D
authors.initials: ND
authors.lastname: Selezneva
authors.forename: S
authors.initials: S
authors.lastname: Voskresenskaya
authors.forename: V
authors.initials: V
authors.lastname: Golimbet
authors.forename: S
authors.initials: S
authors.lastname: Sorbi
authors.forename: R
authors.initials: R
authors.lastname: Duara
authors.forename: S
authors.initials: S
authors.lastname: Gavrilova
authors.forename: P H
authors.initials: PH
authors.lastname: St George-Hyslop
authors.forename: E I
authors.initials: EI
authors.lastname: Rogaev
mesh_terms: D000368:Aged; D000483:Alleles; D000544:Alzheimer Disease / Q000201:enzymology* / Q000453:epidemiology / Q000235:genetics; D001057:Apolipoproteins E / Q000235:genetics / Q000378:metabolism; D004247:DNA / Q000032:analysis / Q000235:genetics; D017931:DNA Primers; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D008297:Male; D009031:Moscow / Q000453:epidemiology; D009864:Ontario / Q000453:epidemiology; D007703:Peptidyl-Dipeptidase A / Q000235:genetics / Q000378:metabolism*; D012307:Risk Factors
chemical_list: D001057:Apolipoproteins E; D017931:DNA Primers; D004247:DNA; D007703:Peptidyl-Dipeptidase A