Association between ApoE epsilon4 and cognitive impairment after stroke.
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.
Wagle
Jørgen
J
Faculty of Medicine, University of Oslo, Oslo, Norway. jowagle@gmail.com
Farner
Lasse
L
Flekkøy
Kjell
K
Wyller
Torgeir Bruun
TB
Sandvik
Leiv
L
Eiklid
Kristin L
KL
Fure
Brynjar
B
Stensrød
Brynhild
B
Engedal
Knut
K
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*
D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D004247:DNA