Crook Zander, Booth Tom, Cox Simon R, Corley Janie, Dykiert Dominika, Redmond Paul, Pattie Alison, Taylor Adele M, Harris Sarah E, Starr John M, Deary Ian J
Department of Psychology, The University of Edinburgh, Edinburgh, United Kingdom.
Centre for Cognitive Ageing and Cognitive Epidemiology, Department of Psychology, The University of Edinburgh, Edinburgh, United Kingdom.
PLoS One. 2018 Feb 16;13(2):e0192604. doi: 10.1371/journal.pone.0192604. eCollection 2018.
In this replication-and-extension study, we tested whether depressive symptoms, neuroticism, and allostatic load (multisystem physiological dysregulation) were related to lower baseline cognitive ability and greater subsequent cognitive decline in older adults, and whether these relationships were moderated by the E4 allele of the apolipoprotein E (APOE) gene. We also tested whether allostatic load mediated the relationships between neuroticism and cognitive outcomes.
We used data from the Lothian Birth Cohort 1936 (n at Waves 1-3: 1,028 [M age = 69.5 y]; 820 [M duration since Wave 1 = 2.98 y]; 659 [M duration since Wave 1 = 6.74 y]). We fitted latent growth curve models of general cognitive ability (modeled using five cognitive tests) with groups of APOE E4 non-carriers and carriers. In separate models, depressive symptoms, neuroticism, and allostatic load predicted baseline cognitive ability and subsequent cognitive decline. In addition, models tested whether allostatic load mediated relationships between neuroticism and cognitive outcomes.
Baseline cognitive ability had small-to-moderate negative associations with depressive symptoms (β range = -0.20 to -0.17), neuroticism (β range = -0.27 to -0.23), and allostatic load (β range = -0.11 to 0.09). Greater cognitive decline was linked to baseline allostatic load (β range = -0.98 to -0.83) and depressive symptoms (β range = -1.00 to -0.88). However, APOE E4 allele possession did not moderate the relationships of depressive symptoms, neuroticism and allostatic load with cognitive ability and cognitive decline. Additionally, the associations of neuroticism with cognitive ability and cognitive decline were not mediated through allostatic load.
Our results suggest that APOE E4 status does not moderate the relationships of depressive symptoms, neuroticism, and allostatic load with cognitive ability and cognitive decline in healthy older adults. The most notable positive finding in the current research was the strong association between allostatic load and cognitive decline.
在这项重复与扩展研究中，我们检验了抑郁症状、神经质以及应激负荷（多系统生理失调）是否与老年人较低的基线认知能力及随后更大的认知衰退相关，以及这些关系是否受载脂蛋白E（APOE）基因的E4等位基因调节。我们还检验了应激负荷是否介导了神经质与认知结果之间的关系。
我们使用了来自1936年洛锡安出生队列的数据（第1 - 3波时的样本量：1028人[平均年龄 = 69.5岁]；820人[自第1波起的平均时长 = 2.98年]；659人[自第1波起的平均时长 = 6.74年]）。我们对APOE E4非携带者和携带者群体拟合了一般认知能力的潜在增长曲线模型（使用五项认知测试进行建模）。在单独的模型中，抑郁症状、神经质和应激负荷被用于预测基线认知能力和随后的认知衰退。此外，模型检验了应激负荷是否介导了神经质与认知结果之间的关系。
基线认知能力与抑郁症状（β范围 = -0.20至 -0.17）、神经质（β范围 = -0.27至 -0.23）和应激负荷（β范围 = -0.11至0.09）呈小到中度的负相关。更大的认知衰退与基线应激负荷（β范围 = -0.98至 -0.83）和抑郁症状（β范围 = -1.00至 -0.88）相关。然而，携带APOE E4等位基因并未调节抑郁症状、神经质和应激负荷与认知能力及认知衰退之间的关系。此外，神经质与认知能力及认知衰退之间的关联并非通过应激负荷介导。
我们的结果表明，在健康老年人中，APOE E4状态并未调节抑郁症状、神经质和应激负荷与认知能力及认知衰退之间的关系。当前研究中最显著的积极发现是应激负荷与认知衰退之间的强关联。
