Edith V. Sullivan, PhD
Edith V. Sullivan,
Abstract & Learning Objectives: Alcohol Use Disorder (AUD) has been a major cause of family, social, and personal strife for centuries, with current prevalence estimates of 14% for 12-month and 29% lifetime AUD. Neuropsychological testing of selective cognitive, sensory, and motor functions complemented with in vivo brain imaging has enabled tracking the consequences of AUD, which follows a dynamic course of development, maintenance, and recovery or relapse. Controlled studies of alcoholism have revealed evidence for disruption of selective functions involving executive, visuospatial, mnemonic, emotional, and balance abilities and brain systems supporting these functions, notably, frontocerebellar, frontostriatal, and frontolimbic circuitry. On a hopeful front, longitudinal study provides convincing evidence for improvement in brain structure and function following sustained sobriety. These discoveries have a strong legacy in INS, starting from its early days when assumptions regarding which brain regions were disrupted relied solely on patterns of functional sparing and impairment deduced from testing. Today’s work using refinements in assessment and multi-modal neuroimaging builds on that legacy, moving the field toward examination of compensatory processes to overcome impaired functions.
After attending this session, learners will be able to:
Recognize that alcohol dependence disrupts selective brain structures and functions
Appreciate that alcoholism-related functional brain changes are a form of neuroadaptation that may underlie dysfunction, making alcoholism a self-perpetuating disorder
Learn that sustained sobriety can result in improvement in brain structure and function, indicative of damage reversal or compensatory mechanisms that can be identified with formal neuropsychological testing and longitudinal, quantitative structural and functional brain imaging
Disclosed support: AA010723, AA012388, AA013521-INIA, AA017168, AA021697-NCANDA
Speaker’s Biography: My commitment to research on human alcoholism began nearly 30 years ago when I joined the Neuroimaging Group at Stanford. I brought to this research collaboration my background as an experimental neuropsychologist and gained from the collaboration experience and expertise as a brain imaging scientist, thus providing complementary understanding about the potential of establishing brain structure-function relations for the first time in alcoholism. This background led to the development of my program of study in alcoholism, focusing on faulty frontocerebellar circuitry as underlying a selective subset of cognitive and motor dysfunctions commonly expressed in alcoholism. In addition to my R01 grant of two decades and now a MERIT Award, I am a recipient of an U01 award for international studies on alcoholism with two INSERM sites in France. In addition, over the past 10 years, I have sought neural mechanisms of alcohol’s untoward effect on brain structure and function using rodent models of chronic exposure to high levels of alcohol. My current work focuses on neural mechanisms of structural and functional connectivity underlying cognitive and motor process and interhemispheric communication in human alcoholism and how comorbidities of HIV infection, hepatitis C infection along with normal aging compound the throes of alcoholism on brain structure, function, and neural circuitry. Most recently, I have embarked on a multi-site consortium study aimed at determining the developmental trajectories of brain, neuropsychological, and emotional development of adolescents and to track deviations from normal trajectories in adolescents who initiate excessive alcohol drinking and measure recovery in those who stop drinking. Coupled with my NIAAA K05 Senior Mentor Award, this integrated research program provides a rich environment for mentoring promising young investigators, who will be the next generation of scientists dedicated to the field of alcohol research.