title: APOE epsilon4 and cognitive decline in older stroke patients with early cognitive impairment.
abstract: BACKGROUND
  Dementia is common post stroke, but the potential role of early cognitive impairment and APOE epsilon4 as risk factors is unclear.
  
  
  METHODS
  Stroke survivors older than 75 years without dementia at 3 months post stroke received a detailed neuropsychological evaluation at 3 and 15 months post stroke, which included the Cambridge Assessment of Mental Disorders in the Elderly (CAMCOG). Early cognitive impairment was diagnosed using the criteria for cognitive impairment/no dementia (vascular CIND). APOE genotype was determined using a standardized method.
  
  
  RESULTS
  One hundred thirty-seven older stroke patients without dementia (mean age 80.6 +/- 4.3, mean CAMCOG score 83.5 +/- 10.4, 68 women) participated in the study, of whom 40 met the criteria for CIND. Stroke patients with one or more APOE epsilon4 alleles were significantly more likely to have CIND (14/40 vs 17/97, odds ratio = 2.5, 95% CI 1.1 to 5.8). Over the 1 year of follow-up, CIND patients with one or more APOE epsilon4 alleles had a mean decline on the total CAMCOG of 2.7 points compared with an improvement of >4 points among patients without APOE epsilon4 (T = 2.9 p = 0.006). CIND patients with an APOE epsilon4 allele also experienced greater decline in memory (T = 2.5, p = 0.015).
  
  
  CONCLUSIONS
  In older stroke patients with early cognitive impairment, the presence of an APOE epsilon4 allele is associated with greater progression of cognitive decline. This has implications for interventions aimed at the secondary prevention of dementia in stroke patients.
authors.affiliation: Institute for Ageing and Health, Wolfson Research Centre, Newcastle General Hospital, Westgate Rd., Newcastle upon Tyne, NE4 6BE, UK. c.g.ballard@ncl.ac.uk
authors.forename: C G
authors.initials: CG
authors.lastname: Ballard
authors.forename: C M
authors.initials: CM
authors.lastname: Morris
authors.forename: H
authors.initials: H
authors.lastname: Rao
authors.forename: J T
authors.initials: JT
authors.lastname: O'Brien
authors.forename: R
authors.initials: R
authors.lastname: Barber
authors.forename: S
authors.initials: S
authors.lastname: Stephens
authors.forename: E
authors.initials: E
authors.lastname: Rowan
authors.forename: A
authors.initials: A
authors.lastname: Gibson
authors.forename: R N
authors.initials: RN
authors.lastname: Kalaria
authors.forename: R A
authors.initials: RA
authors.lastname: Kenny
mesh_terms: D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics*; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D001923:Brain Chemistry / Q000235:genetics; D003072:Cognition Disorders / Q000235:genetics* / Q000503:physiopathology / Q000523:psychology*; D018450:Disease Progression; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005820:Genetic Testing; D006801:Humans; D008297:Male; D008569:Memory Disorders / Q000235:genetics / Q000503:physiopathology / Q000523:psychology; D009483:Neuropsychological Tests; D012307:Risk Factors; D020521:Stroke / Q000150:complications*
chemical_list: D053327:Apolipoprotein E4; D001057:Apolipoproteins E