Critical period for the CNS development
We investigate the role played by environmental risk factors (i.e., psychosocial stress and smoking during pregnancy), maternal biomarkers, and epi/genetic factors on fetal growth and newborn reactivity in conferring vulnerability to developmental psychopathology later in childhood. Considerable data indicate that diverse forms of developmental psychopathology are evident in utero. Maternal stress has been found to be associated with adverse pregnancy outcomes as well as child developmental psychopathology such as anxiety and disruptive disorders. Genetic and maternal serum factors during pregnancy have been linked to susceptibility and transduction of the maternal-fetal response to psychosocial stress. Maternal stress is transduced by serum cortisol levels, and heat-shock proteins are known to chaperone the glucocorticoid receptors at the cellular level (Heitzer et al., 2007). Recent data also demonstrate a strong genetic component in developmental psychopathology, with growing evidence for the important role of the serotonin transporter and glucocorticoid genes. Both genetic and behavioral expression, however, are dependent on a large number of environmental influences, with compelling data to support the presence of gene-environment interactions (Moffitt et al, 2005). To our knowledge, no study to date has prospectively examined the interactions between genes and maternal characteristics that influence gene expression, and serum factors that transduce maternal stress to fetus development and infant reactivity. We intend to explore the role of genetics and epigenetics in moderating the relationship between maternal and infant traits and in conferring future risk for developmental psychopathology in infants.