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Background: Maternal perinatal depression has been shown to have long lasting effects on children's development. Studies have described the relationship of perinatal depression on children's cognition, especially negative effects on intelligence quotient (IQ). However, a recent examination of the current studies to discern the patterns and strength of associations between perinatal depression and child IQ is not available. Objective: The purpose of this systematic review is to discern the effects of perinatal depression, prenatally and within the first 12 months of the postpartum period, on the IQ of the child aged 0–18 years old. Methods: We searched the electronic databases: PubMed and CINAHL. We identified 1633 studies, and included 17 studies in the final review based on pre-determined criteria. After the data was extracted, we assessed the strength of the study using the national heart, lung, and blood institute quality assessment tool for observational cohort and cross-sectional studies. This systematic review had a total sample of 10,757 participants. Results: Across the studies, we identified a relationship between limited maternal responsiveness due to postpartum depression and a decrease in full IQ scores in younger children. Male children were found to be more sensitive to the postpartum depression, resulting in a decrease in IQs, in comparison to female children. Conclusions: Policies should be implemented to identify women suffering from perinatal depression to mitigate the effects of the disorder for both the mother and her child. Significance: Maternal perinatal depression has been shown to have far-reaching effects on children's development. However, a recent examination of the current studies to discern the associations between perinatal depression and child IQ is not available. In this systematic review, we identified a relationship between limited maternal responsiveness due to postpartum depression and a decrease in full IQ scores in younger children. Male children were more sensitive to postpartum depression, resulting in a decrease in IQs, in comparison to female children.. [ABSTRACT FROM AUTHOR]

Up to 50% of children and adolescents in the United States (U.S.) experience sleep problems. While existing research suggests that perceived stress in caregivers is associated with poorer sleep outcomes in children, research on this relationship is often limited to infant and early childhood populations; therefore, we investigated this association in school-age children and adolescents. We used cross-sectional caregiver-reported surveys and applied item response theory (IRT) followed by meta-analysis to assess the relationship between caregiver perceived stress and child sleep disturbance, and moderation of this relationship by child age and the presence of a child mental or physical health condition. We analyzed data from the National Institutes of Health (NIH) Environmental influences on Child Health Outcomes (ECHO) Program, a collaboration of existing pediatric longitudinal cohort studies that collectively contribute a diverse and large sample size ideal for addressing questions related to children's health and consolidating results across population studies. Participants included caregivers of children ages 8 to 16 years from four ECHO cohorts. Caregiver perceived stress was measured using the Perceived Stress Scale (PSS), and child sleep disturbance was assessed using five sleep-related items from the School-Age version of the Child Behavior Checklist (CBCL). Increases in caregiver perceived stress and child mental or physical health condition were independently associated with greater sleep disturbance among children. The findings reinforce the importance of accounting for, and potentially intervening on, the broader family context and children's mental and physical health in the interest of improving sleep health. Highlights: Existing research suggests caregiver perceived stress is associated with worse child sleep outcomes. Data from eight cohorts in the National Institutes of Health (NIH) Environmental influences on Child Health Outcomes (ECHO) program were used. We combined item-level analysis within each cohort with meta-analysis to aggregate results across cohorts. Higher caregiver perceived stress and child health conditions were independently associated with poorer child sleep. Study findings reinforce the importance of the broader family context in the interest of improving sleep health. [ABSTRACT FROM AUTHOR]

As the master regulator in utero, the placenta is core to the Developmental Origins of Health and Disease (DOHaD) hypothesis but is historically understudied. To identify placental gene-trait associations (GTAs) across the life course, we perform distal mediator-enriched transcriptome-wide association studies (TWAS) for 40 traits, integrating placental multi-omics from the Extremely Low Gestational Age Newborn Study. At P < 2.5 × 10 − 6 , we detect 248 GTAs, mostly for neonatal and metabolic traits, across 176 genes, enriched for cell growth and immunological pathways. In aggregate, genetic effects mediated by placental expression significantly explain 4 early-life traits but no later-in-life traits. 89 GTAs show significant mediation through distal genetic variants, identifying hypotheses for distal regulation of GTAs. Investigation of one hypothesis in human placenta-derived choriocarcinoma cells reveal that knockdown of mediator gene EPS15 upregulates predicted targets SPATA13 and FAM214A, both associated with waist-hip ratio in TWAS, and multiple genes involved in metabolic pathways. These results suggest profound health impacts of placental genomic regulation in developmental programming across the life course. The impact of placental transcriptomics on fetal traits throughout development is not well understood. Here, the authors apply distal-SNP-enriched transcriptome-wide association studies to detect genetic contributions, mediated through fetal placental genomics, to developmental programming of complex traits across the life course. [ABSTRACT FROM AUTHOR]

Background: Although survival rates for infants born extremely preterm (gestation < 28 weeks) have improved significantly in recent decades, neurodevelopmental impairment remains a major concern. Children born extremely preterm remain at high risk for cognitive impairment from early childhood to adulthood. However, there is limited evidence on genetic factors associated with cognitive impairment in this population. Methods: First, we used a latent profile analysis (LPA) approach to characterize neurocognitive function at age 10 for children born extremely preterm. Children were classified into two groups: (1) no or low cognitive impairment, and (2) moderate-to-severe cognitive impairment. Second, we performed TOPMed-based genotype imputation on samples with genotype array data (n = 528). Third, we then conducted a genome-wide association study (GWAS) for LPA-inferred cognitive impairment. Finally, computational analysis was conducted to explore potential mechanisms underlying the variant x LPA association. Results: We identified two loci reaching genome-wide significance (p value < 5e-8): TEA domain transcription factor 4 (TEAD4 at rs11829294, p value = 2.40e-8) and syntaxin 18 (STX18 at rs79453226, p value = 1.91e-8). Integrative analysis with brain expression quantitative trait loci (eQTL), chromatin conformation, and epigenomic annotations suggests tetraspanin 9 (TSPAN9) and protein arginine methyltransferase 8 (PRMT8) as potential functional genes underlying the GWAS signal at the TEAD4 locus. Conclusions: We conducted a novel computational analysis by utilizing an LPA-inferred phenotype with genetics data for the first time. This study suggests that rs11829294 and its LD buddies have potential regulatory roles on genes that could impact neurocognitive impairment for extreme preterm born children. [ABSTRACT FROM AUTHOR]

Pre-pregnancy body mass index (BMI) is associated with adverse pregnancy and neonatal health outcomes, with differences in risk observed between sexes. Given that the placenta is a sexually dimorphic organ and critical regulator of development, examining differences in placental mRNA and miRNA expression in relation to pre-pregnancy BMI may provide insight into responses to maternal BMI in utero. Here, genome-wide mRNA and miRNA expression levels were assessed in the placentas of infants born extremely preterm. Differences in expression were evaluated according to pre-pregnancy BMI status (1) overall and (2) in male and female placentas separately. Overall, 719 mRNAs were differentially expressed in relation to underweight status. Unexpectedly, no genes were differentially expressed in relation to overweight or obese status. In male placentas, 572 mRNAs were associated with underweight status, with 503 (70%) overlapping genes identified overall. Notably, 43/572 (8%) of the mRNAs associated with underweight status in male placentas were also gene targets of two miRNAs (miR-4057 and miR-128-1-5p) associated with underweight status in male placentas. Pathways regulating placental nutrient metabolism and angiogenesis were among those enriched in mRNAs associated with underweight status in males. This study is among the first to highlight a sexually dimorphic response to low pre-pregnancy BMI in the placenta. [ABSTRACT FROM AUTHOR]