The Neurobiology of Child Abuse and Neglect

Paradise Lost: The Persistent Biological and Psychiatric Consequences of Child Abuse and Neglect
Brain imaging, neuroendocrine and neurotransmitter studies have revealed the many long-term biological consequences of child abuse and neglect. These changes underlie the increased vulnerability to mood and anxiety disorders in adulthood. Our group and others have demonstrated a number of long term neurobiological consequences of child abuse and neglect including structural and functional brain imaging changes, neuroendocrine and immune alterations.    In particular, alterations in the hypothalamic-pituitary-adrenal (HPA) axis, the major mediator of the mammalian stress response, contribute to the long standing effects of early life trauma.  However, not all exposed individuals demonstrate altered HPA axis physiology, suggesting that genetic variations influence the psychiatric consequences of trauma exposure.  Variants in the genes encoding the CRF R1 receptor, FKBP5, PAC1, oxytocin receptor, and others interact with adverse early environmental factors to predict risk for stress-related psychiatric disorders. Epigenetic mechanisms have now been shown to play a seminal role in mediating the effects of early life stress.  These studies have suggested new molecular targets for drug development, biological risk factors, and predictors of treatment response. Patients with a history of child abuse and neglect exhibit a more severe disease course in terms of earlier age of onset and symptom severity, and exhibit a poorer treatment response to both psychopharmacological and psychotherapeutic treatments. Recognition of the biological consequences and clinical impact of trauma has critical importance for clinical service delivery, treatment research, and public health policy.

Learning Objectives:

  • Discuss how genetic polymorphisms and epigenetics effect psychiatric disease vulnerability
  • Explain how a gene variation effects brain development and function so that the risk of a depressive episode or PTSD is increased
  • Describe how early life experience produces persistent CNS alterations and its implications

Slides in PDF format




Dr. Nemeroff was born in New York City in 1949 and educated in the New York City Public School System. After graduating from the City College of New York in 1970, he enrolled in graduate school at Northeastern University and received a Master’s degree in Biology in 1973. He received his MD and PhD (Neurobiology) from the University of North Carolina at Chapel Hill. His residency training in psychiatry was conducted at both the University of North Carolina and at Duke University, after which he joined the faculty of Duke University. At Duke he was Professor of Psychiatry and Pharmacology and Chief of the Division of Biological Psychiatry before relocating in 1991 to Emory University School of Medicine in Atlanta, Georgia, where he served as the Reunette W. Harris Professor and Chairman of the Department of Psychiatry and Behavioral Sciences until 2008. In 2009 he joined the University of Miami Leonard M. Miller School of Medicine as the Leonard M. Miller Professor and Chairman of the Department of Psychiatry and Behavioral Sciences. His research has concentrated on the biological basis of the major neuropsychiatric disorders, including affective disorders, schizophrenia, and anxiety disorders. His clinical research is focused on the use of genetic, neuroendocrine, neuroimaging and neurochemical methods to comprehensively understand the pathophysiology of depression. In recent years he has uncovered the neurobiological mechanisms that mediate the increased risk for depression in victims of child abuse. He has also contributed to seminal findings in the burgeoning area of research concerning the relationship of depression to cardiovascular disease.

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