Hanna E. Stevens, M.D., Ph.D.
Fellow in Child & Adolescent ADHD
Project Details
Mentor
David Reiss, M.D.
Institution
Yale University School of Medicine
Project
Gene-environment interaction and ADHD: translation between rodent and human models of prenatal stress, genetic risk, and postnatal environment
PROJECT TITLE
Gene-environment interaction and ADHD: translation between rodent and human models of prenatal stress, genetic risk, and postnatal environment
PROJECT SUMMARY
Maternal stress during pregnancy has been associated with ADHD, particularly hyperactive and impulsive symptoms. However, prenatal stress is often correlated with postnatal stress which may influence childhood development. Therefore, it has been difficult to determine whether the risk of ADHD in children exposed to stress in utero develops from prenatal mechanisms or from associated mechanisms that occur after birth. By studying children adopted at birth, contributions of the postnatal environment that may confound traditional studies can be dealt with completely independently.
Dr. Stevens plans to use data from the Early Growth and Development Study (EGDS) which closely examines multiple social and emotional outcomes of adopted children while also collecting diagnostic information about adoptive and birth families; she will evaluate the association of prenatal stress, independent of genetic ADHD risk or postnatal parenting, with ADHD symptoms in adopted children.
To integrate with these data, she will conduct an animal study of prenatal stress. By cross-fostering mice, she will control for risk factors including prenatal stress, genetic vulnerability and postnatal parenting. Pilot data from her lab show that prenatal stress only alters offspring ADHD-like inattention and hyperactivity in combination with a genetic mutation in a brain growth factor receptor. Dr. Stevens will examine neurobiological development in the animal model to determine how inhibitory neuron development and dopaminergic innervations contribute to ADHD-like behavior. Identifying the dysfunction in neural cells that underlies ADHD is a basis by which new, specifically-targeted treatments can be designed for one of the most common behavioral disorders of childhood.
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