Temple University, Department of Psychology and Neuroscience, 1701 N 13th St, Philadelphia, PA 19122, USA.
Temple University, Department of Psychology and Neuroscience, 1701 N 13th St, Philadelphia, PA 19122, USA.
Brain Behav Immun. 2024 Jul;119:908-918. doi: 10.1016/j.bbi.2024.05.012. Epub 2024 May 16.
Accumulating evidence indicates that higher prenatal maternal inflammation is associated with increased depression risk in adolescent and adult-aged offspring. Prenatal maternal inflammation (PNMI) may increase the likelihood for offspring to have lower cognitive performance, which, in turn, may heighten risk for depression onset. Therefore, this study explored the potential mediating role of childhood cognitive performance in the relationship between PNMI and adolescent depressive symptoms in offspring.
Participants included 696 mother-offspring dyads from the Child Health and Development Studies (CHDS) cohort. Biomarkers of maternal inflammation [interleukin (IL)-6, IL-8, IL-1 receptor antagonist (IL-1RA) and soluble TNF receptor-II (sTNF-RII)] were assayed from first (T1) and second trimester (T2) sera. Childhood (ages 9-11) cognitive performance was assessed via standardized Peabody Picture Vocabulary Test (PPVT), a measure of receptive vocabulary correlated with general intelligence. Adolescent (ages 15-17) depressive symptoms were assessed via self-report.
There were no significant associations between T1 biomarkers and childhood PPVT or adolescent depressive symptoms. Higher T2 IL1-RA was directly associated with lower childhood PPVT (b = -0.21, SE = 0.08, t = -2.55, p = 0.01), but not with adolescent depressive symptoms. T2 IL-6 was not directly associated with childhood PPVT, but higher T2 IL-6 was directly associated at borderline significance with greater depressive symptoms in adolescence (b = 0.05, SE = 0.03, t = 1.96, p = 0.05). Lower childhood PPVT predicted significantly higher adolescent depressive symptoms (b = -0.07, SE = 0.02, t = -2.99, p < 0.01). There was a significant indirect effect of T2 IL-1RA on adolescent depressive symptoms via childhood PPVT (b = 0.03, 95 % CI = 0.002-0.03) indicating a partially mediated effect. No significant associations were found with T2 sTNF-RII nor IL-8.
Lower childhood cognitive performance, such as that indicated by a lower PPVT score, represents a potential mechanism through which prenatal maternal inflammation contributes to adolescent depression risk in offspring.
越来越多的证据表明,孕妇产前炎症水平升高与青少年和成年后代的抑郁风险增加有关。产前母体炎症(PNMI)可能增加后代认知表现下降的可能性,而认知表现下降反过来又可能增加抑郁发作的风险。因此,本研究探讨了 PNMI 与后代青少年抑郁症状之间关系中儿童认知表现的潜在中介作用。
参与者包括来自儿童健康与发展研究(CHDS)队列的 696 对母婴对子。从第一(T1)和第二(T2)孕期血清中测定了母体炎症的生物标志物[白细胞介素(IL)-6、IL-8、IL-1 受体拮抗剂(IL-1RA)和可溶性肿瘤坏死因子受体-II(sTNF-RII)]。通过标准化的 Peabody 图片词汇测验(PPVT)评估儿童期(9-11 岁)的认知表现,该测验是一种与一般智力相关的接受性词汇测验。通过自我报告评估青少年(15-17 岁)的抑郁症状。
T1 生物标志物与儿童期 PPVT 或青少年抑郁症状之间没有显著关联。较高的 T2 IL1-RA 与较低的儿童期 PPVT 直接相关(b=-0.21,SE=0.08,t=-2.55,p=0.01),但与青少年抑郁症状无关。T2 IL-6 与儿童期 PPVT 没有直接关联,但较高的 T2 IL-6 与青少年时期的抑郁症状呈边缘显著正相关(b=0.05,SE=0.03,t=1.96,p=0.05)。较低的儿童期 PPVT 显著预测青少年抑郁症状较高(b=-0.07,SE=0.02,t=-2.99,p<0.01)。T2 IL-1RA 通过儿童期 PPVT 对青少年抑郁症状有显著的间接影响(b=0.03,95%CI=0.002-0.03),表明存在部分中介效应。T2 sTNF-RII 和 IL-8 与研究结果无关。
较低的儿童认知表现,如较低的 PPVT 分数所表示的,代表了产前母体炎症导致后代青少年抑郁风险增加的潜在机制。