Department of Neuropsychology and Psychopharmacology, Faculty of Psychology and Neuroscience, Maastricht University, Maastricht, the Netherlands.
Neuropsychology. 2012 Jul;26(4):459-72. doi: 10.1037/a0028685. Epub 2012 May 28.
We investigated suspected longitudinal interaction effects of apolipoprotein E (APOE) genotype and educational attainment on cognitive decline in normal aging.
Our sample consisted of 571 healthy, nondemented adults aged between 49 and 82 years. Linear mixed-models analyses were performed with four measurement time points: baseline, 3-year, 6-year, and 12-year follow-up. Covariates included age at baseline, sex, and self-perceived physical and mental health. Dependent measures were global cognitive functioning (Mini-Mental State Examination; Folstein, Folstein, & McHugh, 1975), Stroop performance (Stroop Color-Word Test; Van der Elst, Van Boxtel, Van Breukelen, & Jolles, 2006a), set-shifting performance (Concept Shifting Test; Van der Elst, Van Boxtel, Van Breukelen, & Jolles, 2006b), cognitive speed (Letter-Digit Substitution Test; Van der Elst, Van Boxtel, Van Breukelen, & Jolles, 2006c), verbal learning (Verbal Learning Test: Sum of five trials; Van der Elst, Van Boxtel, Van Breukelen, & Jolles, 2005), and long-term memory (Verbal Learning Test: Delayed recall).
We found only faint evidence that older, high-educated carriers of the APOE-ε4 allele (irrespective of zygosity) show a more pronounced decline than younger, low-educated carriers and noncarriers (irrespective of educational attainment). Moreover, this outcome was confined to concept-shifting performance and was especially observable between 6- and 12-year follow-ups. No protective effects of higher education were found on any of the six cognitive measures.
We conclude that the combination of APOE-ε4 allele and high educational attainment may be a risk factor for accelerated cognitive decline in older age, as has been reported before, but only to a very limited extent. Moreover, we conclude that, within the cognitive reserve framework, education does not have significant protective power against age-related cognitive decline.
我们研究了载脂蛋白 E（APOE）基因型和教育程度对正常衰老过程中认知能力下降的可疑纵向交互作用。
我们的样本由 571 名年龄在 49 至 82 岁之间的健康、无痴呆的成年人组成。使用四个测量时间点（基线、3 年、6 年和 12 年随访）进行线性混合模型分析。协变量包括基线时的年龄、性别以及自我感知的身体和心理健康。因变量为总体认知功能（简易精神状态检查；Folstein、Folstein 和 McHugh，1975）、Stroop 表现（Stroop 颜色-单词测试；Van der Elst、Van Boxtel、Van Breukelen 和 Jolles，2006a）、定势转移表现（概念转移测试；Van der Elst、Van Boxtel、Van Breukelen 和 Jolles，2006b）、认知速度（字母数字替代测试；Van der Elst、Van Boxtel、Van Breukelen 和 Jolles，2006c）、言语学习（言语学习测试：五次试验总和；Van der Elst、Van Boxtel、Van Breukelen 和 Jolles，2005）和长期记忆（言语学习测试：延迟回忆）。
我们发现，只有微弱的证据表明，年龄较大、受 APOE-ε4 等位基因（无论杂合性如何）影响的高教育程度携带者比年龄较小、受教育程度较低的携带者和非携带者（无论受教育程度如何）表现出更为明显的下降。此外，这种结果仅限于定势转移表现，并且在 6 年至 12 年随访之间尤为明显。我们没有发现较高的教育程度对任何六种认知测量有保护作用。
我们得出结论，APOE-ε4 等位基因和高教育程度的结合可能是导致老年认知能力加速下降的一个风险因素，这与之前的报道一致，但程度非常有限。此外，我们得出结论，在认知储备框架内，教育对与年龄相关的认知能力下降没有显著的保护作用。
