(R01MH093677; Monk & Peterson, B. (MPI))

Children’s neurocognitive development can cast long shadows on their futures, dramatically influencing their occupational functioning and psychosocial adjustment. While it is increasingly recognized that normative varia- tion in early environmental experiences (i.e. parenting style), plays a significant role in shaping cognitive development, evidence indicates that the impact of the environment on cognitive development begins in utero. Two common experiences during pregnancy, psychosocial stress and inadequate micronutrient intake – prominently, iron and zinc, affect outcomes. Prenatal anxiety predicts delayed mental and motor development on the Bayley Scales in infancy, and a reduction in gray matter in the middle temporal lobe based on brain imaging in school-age children. Animal models have demonstrated that antenatal corticosteroid administration is associated with neurocognitive disabilities (i.e. difficulty learning) and structural brain changes such as reduction in hippocampal volume. Infants born to Zinc-deficient mothers show signs of memory impairment. Across both prenatal exposures, what differentiates the animal from the human studies is access to the neonatal brain. The goal of this project is to assess the influence of maternal prenatal stress and poor nutrition on neonatal brain structure and function, and to relate the imaging measures to cognitive outcomes in early childhood. The pro- posed R01 study is a follow-up to an ARRA-funded R01 assessing biopsychosocial stress and nutrition during adolescent pregnancy. Specifically, we have three primary aims to be carried out with pregnant adolescents (ages 15 -19) and their infants: (1) To determine associations between maternal antenatal stress and nutrition, and variation in newborn brain development (from multi-modal imaging). (2) To determine the neural bases of deficits in specific learning and memory tasks, and a general index of cognitive development, associated with prenatal stress and inadequate nutrition. (3) To determine the bidirectional influences between maternal care (i.e. maternal sensitivity and mother-infant attachment style) and infants’ emerging learning and memory capacities. Establishing brain-associated relationships between these prenatal exposures and infant cognition has the potential to help specify the in utero developmental effects of two experiences common to pregnancy, high stress and inadequate nutrition, potentially constraining children’s future learning even before birth. Such results would have significant public health relevance with respect to policy and early intervention approaches. They also could contribute to the identification of exposure-related ‘brain signatures’ to be used for diagnostic and treatment purposes, much as is emerging in imaging studies of depression.

Shkumbin Mustafa