Development, Health and Disease Research Program, University of California, Irvine, California; Department of Pediatrics, University of California, Irvine, California.
Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, Oregon.
Biol Psychiatry Cogn Neurosci Neuroimaging. 2022 Jan;7(1):24-33. doi: 10.1016/j.bpsc.2021.03.007. Epub 2021 Mar 23.
Maternal inflammation during pregnancy can alter offspring brain development and influence risk for disorders commonly accompanied by deficits in cognitive functioning. We therefore examined associations between maternal interleukin 6 (IL-6) concentrations during pregnancy and offspring cognitive ability and concurrent magnetic resonance imaging-based measures of brain anatomy in early childhood. We further examined newborn brain anatomy in secondary analyses to consider whether effects are evident soon after birth and to increase capacity to differentiate effects of pre- versus postnatal exposures.
IL-6 concentrations were quantified in early (12.6 ± 2.8 weeks), mid (20.4 ± 1.5 weeks), and late (30.3 ± 1.3 weeks) pregnancy. Offspring nonverbal fluid intelligence (Gf) was assessed at 5.2 ± 0.6 years using a spatial reasoning task (Wechsler Preschool and Primary Scale of Intelligence-Matrix) (n = 49). T1-weighted magnetic resonance imaging scans were acquired at birth (n = 89, postmenstrual age = 42.9 ± 2.0 weeks) and in early childhood (n = 42, scan age = 5.1 ± 1.0 years). Regional cortical volumes were examined for a joint association between maternal IL-6 and offspring Gf performance.
Average maternal IL-6 concentration during pregnancy was inversely associated with offspring Gf performance after adjusting for socioeconomic status and the quality of the caregiving and learning environment (R = 13%; p = .02). Early-childhood pars triangularis volume was jointly associated with maternal IL-6 and childhood Gf (p < .001). An association also was observed between maternal IL-6 and newborn pars triangularis volume (R = 6%; p = .02).
These findings suggest that the origins of variation in child cognitive ability can, in part, trace back to maternal conditions during the intrauterine period of life and support the role of inflammation as an important component of this putative biological pathway.
孕期母体炎症会改变后代的大脑发育，并增加认知功能障碍相关疾病的风险。因此，我们研究了孕期母体白细胞介素 6（IL-6）浓度与后代认知能力以及儿童早期基于磁共振成像的大脑解剖结构之间的关联。我们在二次分析中进一步研究了新生儿的大脑解剖结构，以考虑这些影响是否在出生后不久就显现出来，并提高区分产前和产后暴露影响的能力。
在孕早期（12.6±2.8 周）、孕中期（20.4±1.5 周）和孕晚期（30.3±1.3 周）测量 IL-6 浓度。在 5.2±0.6 岁时，使用空间推理任务（Wechsler 学前和小学智力量表-矩阵）（n=49）评估后代的非言语流体智力（Gf）。在出生时（n=89，孕龄=42.9±2.0 周）和儿童早期（n=42，扫描年龄=5.1±1.0 岁）采集 T1 加权磁共振成像扫描。研究了母体 IL-6 与后代 Gf 表现之间的联合关联与皮质区域体积的关系。
调整社会经济地位以及育儿和学习环境的质量后，孕期母体 IL-6 浓度的平均值与后代的 Gf 表现呈负相关（R=13%，p=0.02）。儿童早期三角部容积与母体 IL-6 和儿童 Gf 呈联合相关（p<0.001）。也观察到母体 IL-6 与新生儿三角部容积之间存在关联（R=6%，p=0.02）。
这些发现表明，儿童认知能力的差异部分可以追溯到宫内生命期间的母体状况，并支持炎症作为这一潜在生物学途径的重要组成部分的作用。
