Adopted individuals in large-scale population based cohorts can be leveraged to partition maternal genetic effects into prenatal and postnatal components, helping elucidate the underlying mechanisms behind these associations, and for diseases, yielding important information regarding the optimal timing of interventions.

Prenatal stress is transmitted to infant development through cortisol, which imparts sex-specific effects on the development and connectivity of the amygdalae.

Early moderate consumption of alcohol in pregnancy was sufficient to disrupt the fetal epigenome in newborn mice, and high folate maternal diets had a mitigating effect.

A novel, translational mouse model of prenatal methadone exposure was developed and a longitudinal assessment of offspring revealed impairments in physical, behavioral, and neuronal development.

In wild baboons, a female's adverse early experiences can influence her offspring's survival years after the original adversity was experienced.

Gene analyses reveal the abnormal DNA methylation and expression of the genes essential for spermatogenesis as a cause of spermatogenic defects in offspring induced by maternal exposure of a chemical.

Prenatal ethanol exposure results in aberrant tangential migration by altering NKCC1-mediated chloride homeostasis that can be mitigated by bumetanide.

Targeting the mothers, and other household members, of newborns with a mixture of respiratory syncytial virus (RSV) vaccines is both efficient and effective at reducing RSV hospitalizations.

Ts65dn mice exhibit structural, functional, molecular, and genetic alterations that are modulated but unrecovered by prenatal chronic GTE-EGCG, highlighting the importance of holistic studies to understand complex disorders and treatments.

A cross-fostered population of mice reveals loci on offspring chromosomes 5 and 7 that modify the behaviour of their mothers, along with evidence of coadaptation between offspring and parental traits.