title: APOE epsilon 4 allele predicts faster cognitive decline in mild Alzheimer disease.
abstract: OBJECTIVE
  To determine whether APOE epsilon 4 predicts rate of cognitive change in incident and prevalent Alzheimer disease (AD).
  
  
  METHODS
  Individuals were recruited from two longitudinal cohort studies-the Washington Heights and Inwood Columbia Aging Project (WHICAP; population-based) and the Predictors Study (clinic-based)--and were followed for an average of 4 years. Three samples of participants diagnosed with AD, with diverse demographic characteristics and baseline cognitive functioning, were studied: 1) 199 (48%) of the incident WHICAP cases; 2) 215 (54%) of the prevalent WHICAP cases; and 3) 156 (71%) of the individuals diagnosed with AD in the Predictors Study. Generalized estimating equations were used to test whether rate of cognitive change, measured using a composite cognitive score in WHICAP and the Mini-Mental State Examination in Predictors, varied as a function of epsilon 4 status in each sample.
  
  
  RESULTS
  The presence of at least one epsilon 4 allele was associated with faster cognitive decline in the incident population-based AD group (p = 0.01). Parallel results were produced for the two prevalent dementia samples only when adjusting for disease severity or excluding the most impaired participants from the analyses.
  
  
  CONCLUSIONS
  APOE epsilon 4 may influence rate of cognitive decline most significantly in the earliest stages of Alzheimer disease.
authors.affiliation: Cognitive Neuroscience Division of the Gertrude H. Sergievsky Center, Columbia University Medical Center, New York, NY 10032, USA.
authors.forename: S
authors.initials: S
authors.lastname: Cosentino
authors.forename: N
authors.initials: N
authors.lastname: Scarmeas
authors.forename: E
authors.initials: E
authors.lastname: Helzner
authors.forename: M M
authors.initials: MM
authors.lastname: Glymour
authors.forename: J
authors.initials: J
authors.lastname: Brandt
authors.forename: M
authors.initials: M
authors.lastname: Albert
authors.forename: D
authors.initials: D
authors.lastname: Blacker
authors.forename: Y
authors.initials: Y
authors.lastname: Stern
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000544:Alzheimer Disease / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D053327:Apolipoprotein E4 / Q000235:genetics*; D003072:Cognition Disorders / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D015331:Cohort Studies; D004252:DNA Mutational Analysis; D018450:Disease Progression; D005260:Female; D005787:Gene Frequency / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005820:Genetic Testing; D005838:Genotype; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D008569:Memory Disorders / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D011110:Polymorphism, Genetic / Q000235:genetics; D011446:Prospective Studies; D013997:Time Factors
chemical_list: D053327:Apolipoprotein E4