Norwegian Centre for Ageing and Health, Specialist Service in Psychiatry, Vestfold Hospital Trust, Norway.
Int J Geriatr Psychiatry. 2010 Aug;25(8):833-42. doi: 10.1002/gps.2425.
To examine the relationship between the ApoE epsilon4 allele and cognitive impairment 13 months after stroke.
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.
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.
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.
研究载脂蛋白 E ɛ4 等位基因与卒中后 13 个月认知障碍的关系。
104 例卒中康复患者平均在入院后 18 天进行认知测试，13 个月后使用重复神经心理状态评估量表（RBANS）再次进行测试。采用二变量和逻辑回归分析对卒中后 13 个月认知障碍（定义为 RBANS 总分低于 77.5 分）的以下潜在危险因素进行分析：载脂蛋白 E 基因型、社会人口学变量、卒中前认知减退（老年认知减退简易问卷（IQCODE））、血管因素、病灶特征和神经损伤（国立卫生研究院卒中量表（NIHSS））。分析不同载脂蛋白 E 基因型患者的一般认知表现（卒中前、基线和随访）的差异，最后比较载脂蛋白 E ɛ4 携带者和非携带者在 13 个月期间各认知领域的表现变化差异。
13 个月时认知障碍的显著危险因素为载脂蛋白 E ɛ4、卒中前认知减退（IQCODE3.44+）、既往卒中及神经损伤（NIHSS 总分>5）。在基线和随访时发现载脂蛋白 E 基因型与整体卒中后认知功能之间存在显著的剂量依赖性关系，但在卒中前无此关系。与非携带者相比，载脂蛋白 E ɛ4 携带者在与语言学习和记忆相关的测试中表现出明显的下降。
载脂蛋白 E ɛ4 等位基因是卒中后 13 个月认知障碍的独立危险因素，与语言学习和记忆相关任务的认知衰退进展相关。
