title: A comprehensive genetic association study of Alzheimer disease in African Americans.
abstract: OBJECTIVE
  To evaluate the association of genetic variation with late-onset Alzheimer disease (AD) in African Americans, including genes implicated in recent genome-wide association studies of whites.
  
  
  METHODS
  We analyzed a genome-wide set of 2.5 million imputed markers to evaluate the genetic basis of AD in an African American population.
  
  
  METHODS
  Five hundred thirteen well-characterized African American AD cases and 496 cognitively normal African American control subjects.
  
  
  METHODS
  Data were collected from multiple sites as part of the Multi-Institutional Research on Alzheimer Genetic Epidemiology (MIRAGE) Study and the Henry Ford Health System as part of the Genetic and Environmental Risk Factors for Alzheimer Disease Among African Americans (GenerAAtions) Study.
  
  
  RESULTS
  Several significant single-nucleotide polymorphisms (SNPs) were observed in the region of the apolipoprotein E gene (APOE). After adjusting for the confounding effects of APOE genotype, one of these SNPs, rs6859 in PVRL2, remained significantly associated with AD (P = .0087). Association was also observed with SNPs in CLU, PICALM, BIN1, EPHA1, MS4A, ABCA7, and CD33, although the effect direction for some SNPs and the most significant SNPs differed from findings in data sets consisting of whites. Finally, using the African American genome-wide association study data set as a discovery sample, we obtained suggestive evidence of association with SNPs for several novel candidate genes.
  
  
  CONCLUSIONS
  Some genes contribute to AD pathogenesis in both white and African American cohorts, although it is unclear whether the causal variants are the same. A larger African American sample will be needed to confirm novel gene associations, which may be population specific.
authors.affiliation: Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA.
authors.forename: Mark W
authors.initials: MW
authors.lastname: Logue
authors.forename: Matthew
authors.initials: M
authors.lastname: Schu
authors.forename: Badri N
authors.initials: BN
authors.lastname: Vardarajan
authors.forename: Jacki
authors.initials: J
authors.lastname: Buros
authors.forename: Robert C
authors.initials: RC
authors.lastname: Green
authors.forename: Rodney C P
authors.initials: RC
authors.lastname: Go
authors.forename: Patrick
authors.initials: P
authors.lastname: Griffith
authors.forename: Thomas O
authors.initials: TO
authors.lastname: Obisesan
authors.forename: Rhonna
authors.initials: R
authors.lastname: Shatz
authors.forename: Amy
authors.initials: A
authors.lastname: Borenstein
authors.forename: L Adrienne
authors.initials: LA
authors.lastname: Cupples
authors.forename: Kathryn L
authors.initials: KL
authors.lastname: Lunetta
authors.forename: M Daniele
authors.initials: MD
authors.lastname: Fallin
authors.forename: Clinton T
authors.initials: CT
authors.lastname: Baldwin
authors.forename: Lindsay A
authors.initials: LA
authors.lastname: Farrer
mesh_terms: D001741:Black or African American / Q000235:genetics*; D017668:Age of Onset; D000368:Aged; D000544:Alzheimer Disease / Q000453:epidemiology* / Q000235:genetics*; D053329:Apolipoprotein E2 / Q000235:genetics; D053318:Apolipoprotein E3 / Q000235:genetics; D053327:Apolipoprotein E4 / Q000235:genetics; D016022:Case-Control Studies; D005260:Female; D020022:Genetic Predisposition to Disease; D055106:Genome-Wide Association Study; D005838:Genotype; D006801:Humans; D008297:Male; D020641:Polymorphism, Single Nucleotide / Q000235:genetics
chemical_list: D053329:Apolipoprotein E2; D053318:Apolipoprotein E3; D053327:Apolipoprotein E4