Epigenetic Regulation of Infant Neurobehavioral Outcomes

Abstract

During fetal development and early infancy, environmental signals can induce epigenetic changes that alter neurobehavioral development and later-life mental health. Several neurodevelopmental genetic diseases influence epigenetic regulatory genes and genomic imprinting. Recently, brain epigenetic marks have been involved in idiopathic neurodevelopmental disorders, including autism spectrum disorders. The placenta is an important regulator of the intrauterine environment that links maternal and fetal nervous systems. Placental epigenetic signatures have been associated with the neurodevelopment of healthy newborns quantified through the Neonatal Intensive Care Unit Network Neurobehavioral Scales (NNNS). Associations have been observed for DNA methylation of genes involved in cortisol <i>(NR3C1, HSD11B)</i>, serotonin <i>(HTR2A)</i>, and metabolic <i>(LEP)</i> pathways. Dysregulation of imprinted genes and microRNAs has also been associated with neurobehavior assessed by NNNS. Further analysis is needed to characterize the mechanisms by which the epigenome influences neurodevelopment and the connection between this dysregulation and mental health disorders. In the future, epigenetic marks could serve as functional biomarkers of mental health and cognitive function.