title: The apolipoprotein E epsilon4 allele increases the odds of chronic cerebral infarction [corrected] detected at autopsy in older persons.
abstract: OBJECTIVE
  Studies investigating the relation of the apolipoprotein E (apoE) epsilon4 allele to clinical stroke and to vascular changes on magnetic resonance imaging have been conflicting. Little data are available regarding the relation of apoE epsilon4 to cerebral infarctions documented on postmortem examination.
  
  
  METHODS
  We studied the apoE epsilon4 allele in 214 deceased members of the Religious Orders Study, a longitudinal clinical-pathologic study of aging and Alzheimer disease. The apoE genotype was determined using DNA from lymphocytes. Brains were removed a median of 5 hours (interquartile range, 5.5) after death. At postmortem examination, age, location, and size of macroscopic chronic cerebral infarctions were recorded from 1-cm coronal slabs after paraformaldehyde fixation. We also examined 20-microm paraffin-embedded sections of midfrontal and calcarine cortex for amyloid angiopathy on a scale of 1 to 4.
  
  
  RESULTS
  Subjects included 96 males and 118 females with a mean age at death of 86 years (SD, 7). Sixty-five subjects (30.4%) had at least 1 apoE epsilon4 allele and 76 (35.5%) exhibited cerebral infarctions. More than 74% of the subjects exhibited amyloid angiopathy with a mean score of 1.4+/-1.2. After controlling for age and sex, apoE epsilon4 increased the odds of cerebral infarction by 2.3-fold (95% CI, 1.2 to 4.2). apoE epsilon4 increased the odds of cortical 3.2-fold (95% CI, 1.3 to 7.7) and subcortical infarctions 2.3-fold (95% CI, 1.2 to 4.5). The effect was unchanged after accounting for amyloid angiopathy.
  
  
  CONCLUSIONS
  apoE epsilon4 increases the odds of chronic cerebral infarction detected at autopsy in older persons.
authors.affiliation: Rush AD Center and Rush Institute for Healthy Aging, Rush University Medical Center, Chicago, Ill, USA. Julie_A_Schneider@rush.edu
authors.forename: J A
authors.initials: JA
authors.lastname: Schneider
authors.forename: J L
authors.initials: JL
authors.lastname: Bienias
authors.forename: R S
authors.initials: RS
authors.lastname: Wilson
authors.forename: E
authors.initials: E
authors.lastname: Berry-Kravis
authors.forename: D A
authors.initials: DA
authors.lastname: Evans
authors.forename: D A
authors.initials: DA
authors.lastname: Bennett
mesh_terms: D000368:Aged; D000483:Alleles; D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics*; D016657:Cerebral Amyloid Angiopathy / Q000235:genetics / Q000473:pathology; D002544:Cerebral Infarction / Q000145:classification / Q000235:genetics* / Q000473:pathology; D002908:Chronic Disease; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D014652:Vascular Diseases / Q000235:genetics
chemical_list: D053327:Apolipoprotein E4; D001057:Apolipoproteins E