Cognitive impairment and the role of the ApoE epsilon4-allele after stroke--a 13 months follow-up study.

OBJECTIVE:To examine the relationship between the ApoE epsilon4 allele and cognitive impairment 13 months after stroke. METHODS:One hundred four stroke rehabilitation patients were cognitively tested on average 18 days after hospital admission and again 13 months later with the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). The following potential risk factors for post-stroke cognitive impairment (defined by a RBANS total index score below 77.5 points) at 13 months follow-up were analyzed in bivariate and logistic regression analyses: ApoE-genotype, socio-demographic variables, pre-stroke cognitive reduction (The Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE)), vascular factors, lesion characteristics, and neurological impairment (The National Institute of Health Stroke Scale (NIHSS)). Differences in general cognitive performance (pre-stroke, baseline, and follow-up) across patients with different ApoE-genotypes were analyzed, and lastly differences between epsilon4-carriers and non-carriers for changes in performance in various cognitive domains over the 13 months period were examined. RESULTS:Significant risk factors for cognitive impairment at 13 months were ApoE epsilon4, pre-stroke cognitive reduction (IQCODE 3.44+), previous stroke, and neurological impairment (NIHSS Total Score >5). A significant dose-dependent effect of the ApoE-genotype in relation to overall post-stroke cognitive functioning was found at baseline and follow-up, but not pre-stroke. The epsilon4 carriers showed a significant decline in tests related to verbal learning and memory compared to the non-carriers. CONCLUSIONS:The ApoE epsilon4-allele constitutes an independent risk factor for cognitive impairment at 13 months post-stroke, and is associated with progression of cognitive decline in tasks related to verbal learning and memory.