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.

Epigenetic reprogramming by LSD1/KDM1A acts at fertilization in mice to enable embryogenesis and prevent behavioural abnormalities.

Maternal obesity alters the fetal cardiac and serum lipidome, promoting early fetal cardiac metabolic maturation, with evidence that the female heart lipidome is more responsive to an in utero obesogenic environment.

Imprinted gene expression is set up during a critical window of early embryonic development, by the translation of parental imprints by oocyte-supplied Smchd1 into allele-specific gene silencing.

Zdbf2 is a paternally expressed gene that is mainly expressed in the hypothalamus and promotes appetite and body weight gain in neonates.

Mice exposed to complex early adversity show similar diffusion MRI changes to those reported in humans and sex-specific changes in connectivity that differentially affect contextual deficits in males and females.

The PVN-mPFC OT circuit is an important target for the treatment of disorders related to early adverse experiences.

Transient hormonal alterations during early critical developmental periods can have a crucial and long-lasting effect on lifespan in mice.

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.