title: Incidence of Alzheimer disease in a biracial urban community: relation to apolipoprotein E allele status.
abstract: BACKGROUND
  Few studies compare Alzheimer disease (AD) incidence among black and white subjects.
  
  
  OBJECTIVE
  To estimate incidence and the effect of the apolipoprotein E (APOE) epsilon4 allele in these races.
  
  
  METHODS
  Population-based study of disease incidence using a random, stratified sample.
  
  
  METHODS
  A geographically defined community of 3 adjacent neighborhoods in Chicago, Ill.
  
  
  METHODS
  A total of 6158 persons (78.7% overall; 80.5% of the black subjects and 74.6% of the white subjects) participated; 4.1 years later, persons initially free of AD were sampled for clinical evaluation for disease incidence (overall 842 persons [74.8%] participated; 67.6% of the black subjects and 81.9% of the white subjects).
  
  
  METHODS
  None.
  
  
  METHODS
  Incident, clinically diagnosed AD.
  
  
  RESULTS
  The effect of the APOE epsilon4 allele on the risk of AD differed strongly for black and white subjects. Among white subjects, the presence of the APOE epsilon4 allele was associated with a 2.73-fold (95% confidence interval [CI], 1.40-5.32) increase in risk while among black subjects there was no increase in risk (odds ratio, 1.02; 95% confidence interval, 0.39-2.68). Black race was associated with a nonsignificantly increased risk of AD with an odds ratio of 1.84 (95% CI, 0.73-4.66) if APOE and its interaction with race are considered, and an odds ratio of 1.28 (95% CI, 0.54-2.98) if they are not. The incidence of AD was 1.45% (95% CI, 0.89%-2.01%) per year among persons 65 to 74 years old, 4.73% (95% CI, 3.83%-5.64%) among those 75 to 84 years old, and 9.11% (95% CI, 7.36%-10.9%) among those 85 years and older.
  
  
  CONCLUSIONS
  Apolipoprotein E epsilon4 led to increased risk of AD among white subjects but not black subjects.
authors.affiliation: Rush Institute on Healthy Aging, Chicago, IL, USA. devans2@rush.edu
authors.forename: Denis A
authors.initials: DA
authors.lastname: Evans
authors.forename: David A
authors.initials: DA
authors.lastname: Bennett
authors.forename: Robert S
authors.initials: RS
authors.lastname: Wilson
authors.forename: Julia L
authors.initials: JL
authors.lastname: Bienias
authors.forename: Martha Clare
authors.initials: MC
authors.lastname: Morris
authors.forename: Paul A
authors.initials: PA
authors.lastname: Scherr
authors.forename: Liesi E
authors.initials: LE
authors.lastname: Hebert
authors.forename: Neelum
authors.initials: N
authors.lastname: Aggarwal
authors.forename: Laurel A
authors.initials: LA
authors.lastname: Beckett
authors.forename: Rajiv
authors.initials: R
authors.lastname: Joglekar
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Berry-Kravis
authors.forename: Julie
authors.initials: J
authors.lastname: Schneider
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000453:epidemiology* / Q000208:ethnology / Q000235:genetics*; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics*; D044383:Black People; D016021:Epidemiologic Studies; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D015994:Incidence; D008297:Male; D012307:Risk Factors; D014505:Urban Population; D044465:White People
chemical_list: D053327:Apolipoprotein E4; D001057:Apolipoproteins E