title: Association between ApoE epsilon4 and cognitive impairment after stroke.
abstract: OBJECTIVE
  The understanding of the contribution of genetic factors to cognitive impairment after stroke is incomplete. The aim of the study was to examine whether the apolipoprotein E epsilon4 allele (ApoE epsilon4) is a risk factor for cognitive impairment in the early phase after stroke.
  
  
  METHODS
  The sample comprised 152 Norwegian stroke rehabilitation inpatients (mean age 76.8 years, SD 10.5) examined at a mean of 18.3 days (SD 13.4) after hospital admission. Post-stroke cognitive impairment was assessed with the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). The following proposed risk factors were analysed: ApoE genotype, demographics (age, sex, education), pre-stroke cognitive reduction [Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE)], pre-stroke vascular factors (including previous stroke), stroke characteristics (type, location), and neurological stroke-related impairment [National Institutes of Health Stroke Scale (NIHSS)]. Cognitive impairment was defined as an RBANS total index score < or =1.5 SD below the mean. Multiple logistic regression analyses were performed to find risk factors for post-stroke cognitive impairment.
  
  
  RESULTS
  Four variables were found to be independent risk factors for cognitive impairment after stroke: ApoE epsilon4 (OR = 3.7; 95% CI = 1.2-11.6), IQCODE score > or =3.44 (OR = 9.2; 95% = CI 2.3-37.2), total or partial anterior stroke syndromes (OR = 3.2; 95% CI = 1.3-8.0), and NIHSS total score >5 (OR = 7.3; 95% CI = 2.7-19.7). No association between ApoE epsilon4 and pre-stroke cognitive reduction (IQCODE) was found.
  
  
  CONCLUSIONS
  The presence of one or two ApoE epsilon4 alleles may be a significant independent risk factor for cognitive impairment in the early phase after stroke.
authors.affiliation: Faculty of Medicine, University of Oslo, Oslo, Norway. jowagle@gmail.com
authors.forename: Jørgen
authors.initials: J
authors.lastname: Wagle
authors.forename: Lasse
authors.initials: L
authors.lastname: Farner
authors.forename: Kjell
authors.initials: K
authors.lastname: Flekkøy
authors.forename: Torgeir Bruun
authors.initials: TB
authors.lastname: Wyller
authors.forename: Leiv
authors.initials: L
authors.lastname: Sandvik
authors.forename: Kristin L
authors.initials: KL
authors.lastname: Eiklid
authors.forename: Brynjar
authors.initials: B
authors.lastname: Fure
authors.forename: Brynhild
authors.initials: B
authors.lastname: Stensrød
authors.forename: Knut
authors.initials: K
authors.lastname: Engedal
mesh_terms: D000368:Aged; D001037:Aphasia / Q000209:etiology / Q000503:physiopathology; D053327:Apolipoprotein E4 / Q000235:genetics*; D001057:Apolipoproteins E / Q000235:genetics; D002545:Brain Ischemia / Q000150:complications; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000235:genetics; D002543:Cerebral Hemorrhage / Q000150:complications; D002560:Cerebrovascular Circulation / Q000502:physiology; D003072:Cognition Disorders / Q000209:etiology* / Q000235:genetics*; D004247:DNA / Q000235:genetics; D005260:Female; D005838:Genotype; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009483:Neuropsychological Tests; D011597:Psychomotor Performance / Q000502:physiology; D012307:Risk Factors; D020521:Stroke / Q000150:complications* / Q000209:etiology / Q000235:genetics*
chemical_list: D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D004247:DNA