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Genes, brain, and environment as direct and interactive predictors of antisocial behavior from early childhood to young adulthood"
Developmental Brown Bag

Luke Hyde, Assistant Professor of Psychology, University of Michigan

Monday, October 29, 2012, 12:00 pm – 1:00 pm
3447 East Hall

Event Information

Abstract: Antisocial behavior (AB), including physical and sexual aggression, destruction of property, theft, and violation of serious rules, has been of particular interest to researchers and the general public because of its large cost to society and negative impact on perpetrators and victims, its chronic nature and trajectory, and the difficulty in preventing and treating AB. Although recent views of AB have emphasized the complex interplay between biology and the environment (Jaffee et al., 2005; Reiss, 2005; Rutter, 1997), little empirical work has connected genetic variability, neural reactivity and environmental risk in understanding the development of AB in early adulthood. In this talk I will briefly outline a multi-method, multi-level developmental psychopathology approach for studying this disorder and will highlight some of my past research in this area. Next, I’ll focus on a recent study that sought to advance our understanding of AB in an ethnically diverse sample of 310 young men followed prospectively from age 1.5 to age 20 through measurement of amygdala reactivity to threat, variability in genes affecting serotonin signaling, cumulative environmental risk during early childhood and early adolescence, and measures of AB during adolescence and at age 20. Within this study, we found that AB across adolescence and at age 20 was related to lower amygdala reactivity to an emotional faces paradigm, regardless of the level of callous traits also present. We also found that variants of serotonin genes previously linked to lower amygdala reactivity were related to callous traits as well as AB in the presence of high callousness. Though we tested Imaging Genetics (Hariri & Weinberger, 2003) and Imaging Gene by Environment Interaction (Hyde, et al., 2011) models, we found little support for these models with these variables in this sample. Results highlight the difficulty in testing realistic but complex models of the interactions between genes, brain and environment in understanding AB and highlight the role of amygdala reactivity in AB. I will close with ideas for my future research at UM.

Bio: Luke Hyde graduated with a B.A. cum laude from Williams College and received his Ph.D. in Clinical and Developmental Psychology with a concentration in Cognitive Neuroscience at the University of Pittsburgh where he was mentored by Daniel Shaw and Ahmad Hariri. He is currently an Assistant Professor in Psychology in the Clinical and Developmental areas at the University of Michigan. His developmental psychopathology research focuses on the interaction of environments (e.g., parenting, neighborhood danger) with biology (e.g., genes, neural function) in predicting later behavior, especially antisocial behaviors, from toddlerhood to adolescence.



Department of Psychology
University of Michigan
1012 East Hall
530 Church Street
Ann Arbor, MI
48109-1043
734 764 2580 voice
734 764 3520 fax

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