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Most evidence of the association between maternal depression and children's development is limited by being cross-sectional. To date, few studies have modelled trajectories of maternal depressive symptoms from pregnancy through the early postpartum years and examined their association with social emotional and behavior functioning in preschool children. The objectives of this study were to: 1) identify distinct groups of women defined by their trajectories of depressive symptoms across four time points from mid-pregnancy to one year postpartum; and 2) examine the associations between these trajectories and child internalizing and externalizing behaviors.We analyzed data from the All Our Families (AOF) study, a large, population based pregnancy cohort of mother-child dyads in Alberta, Canada. The AOF study is an ongoing pregnancy cohort study designed to investigate relationships between the prenatal and early life period and outcomes for children and mothers. Maternal depressive symptoms were assessed using the Edinburgh Postnatal Depression Scale. Children's behavioral functioning at age 3 was assessed using the Behavior Scales developed for the Canadian National Longitudinal Survey of Children and Youth. Longitudinal latent class analysis was conducted to identify trajectories of women's depressive symptoms across four time points from pregnancy to 1 year postpartum. We used multivariable logistic regression to assess the relationship between trajectories of maternal depressive symptoms and children's behavior, while adjusting for other significant maternal, child and psychosocial factors.1983 participants met eligibility criteria. We identified four distinct trajectories of maternal depressive symptoms: low level (64.7%); early postpartum (10.9%); subclinical (18.8%); and persistent high (5.6%). In multivariable models, the proportion of children with elevated behavior symptoms was highest for children whose mothers had persistent high depressive symptoms, followed by mothers with moderate symptoms (early postpartum and subclinical trajectories) and lowest for minimal symptoms. After accounting for demographic, child and psychosocial factors, the relationships between depression trajectories and child hyperactivity/inattention, physical aggression (subclinical trajectory only) and separation anxiety symptoms remained significant.These findings suggest both externalizing and internalizing children's behaviors are associated with prolonged maternal depressive symptoms. There is a good case for the need to move beyond overly simplistic clinical cutoff approaches of depressed/not depressed in screening for perinatal depression. Women with elevated depressive symptoms at clinical and subclinical levels need to be identified, provided with evidence-based treatment, and monitored with repeat screening to improve maternal mental health outcomes and reduce the risk of associated negative outcomes on children's early social-emotional and behavior development.

The gestational state is a period of particular vulnerability to diseases that affect maternal and fetal health. Stress during gestation may represent a powerful influence on maternal mental health and offspring brain plasticity and development. Here we show that the fetal transcriptome, through microRNA (miRNA) regulation, responds to prenatal stress in association with epigenetic signatures of psychiatric and neurological diseases. Pregnant Long-Evans rats were assigned to stress from gestational days 12 to 18 while others served as handled controls. Gestational stress in the dam disrupted parturient maternal behaviour and was accompanied by characteristic brain miRNA profiles in the mother and her offspring, and altered transcriptomic brain profiles in the offspring. In the offspring brains, prenatal stress upregulated miR-103, which is involved in brain pathologies, and downregulated its potential gene target Ptplb. Prenatal stress downregulated miR-145, a marker of multiple sclerosis in humans. Prenatal stress also upregulated miR-323 and miR-98, which may alter inflammatory responses in the brain. Furthermore, prenatal stress upregulated miR-219, which targets the gene Dazap1. Both miR-219 and Dazap1 are putative markers of schizophrenia and bipolar affective disorder in humans. Offspring transcriptomic changes included genes related to development, axonal guidance and neuropathology. These findings indicate that prenatal stress modifies epigenetic signatures linked to disease during critical periods of fetal brain development. These observations provide a new mechanistic association between environmental and genetic risk factors in psychiatric and neurological disease.