Program & Abstract Book - EPFL Latsis Symposium 2009
Program & Abstract Book - EPFL Latsis Symposium 2009 Program & Abstract Book - EPFL Latsis Symposium 2009
EPFL Latsis Symposium 2009: Understanding Violence S-13 38 February 11-13 2009 ge t t i n g t h e p h e n o t y p e s r i g h t : th e e s s e n t i a l i n g r e D i e n t t o u n D e r s t a n D i n g a e t i o l o g i c a l m e c h a n i s m s a n D D e v e l o p i n g e f f e c t i v e t r e a t m e n t s Hodgins, Sheilagh Institute of Psychiatry King’s College, University of London UK The population of individuals who as adults engage in persistent physical violence towards others is not homogeneous. The available evidence suggests that it includes at least three sub-groups. While all of the sub-groups display an early-onset pattern of antisocial behaviour that remains stable across the life-span, the sub-groups differ in behaviour, mental disorders, personality traits, emotion processing, cognitive abilities, attentional processes, and stress reactivity. These differences emerge at an early age and the sub-groups appear to remain distinct from childhood through adulthood. Yet, knowledge of the development of these sub-groups of individuals who become persistent violent offenders is very limited. Consequently, inadequate characterization of participants in investigations of genes that confer vulnerability for persistent violent behaviour, of brain structure and function, and in studies of the links between specific genes and brain structure and function limits the meaningfulness of the results. Accurate characterization of sub-groups of persistently violent individuals, at each developmental stage, is necessary in order to elucidate the complex mechanisms through the course of development that lead to an adult who persistently engages in violent behaviour towards others. Without understanding these developmental mechanisms, the establishment of effective prevention and treatment programmes is not likely.
EPFL Latsis Symposium 2009: Understanding Violence S-14 Abstracts for Speakers mu l t i m o D a l c h a r a c t e r i z a t i o n o f g e n e t i c r i s k m e c h a n i s m s f o r impulsive a g g r e s s i o n Buckholtz, Joshua W. Neuroscience Vanderbilt Brain Institute Department of Psychology Vanderbilt University, Nashville, TN USA It has long been noted that antisocial traits and behaviors tend to run in families. More recently, family, adoption and twin studies have confirmed the heritability of antisocial aggression, demonstrating that genetic influences are in great part responsible for its intergenerational transmission. However, even for the most promising candidate gene for antisociality – MAOA – statistical genetic associations to disorders of aggression are often weak and inconsistent. By contrast, a robust and replicated gene-by-environment interaction has been demonstrated between childhood maltreatment and allelic variation in the MAOA promoter¸ with markedly higher rates of antisocial behavior found in male carriers of a low expressing allele (MAOA-L) who have been abused as children. I will present neuroimaging evidence that the MAOA-L allele is associated with profound alterations in the structure and function of, and connectivity between, key neural nodes for affect processing, emotion regulation and social evaluation. This “socio-affective scaffold” – comprised of amygdala, rostral cingulate, and medial prefrontal cortex – appears to be uniquely vulnerable to the effect of elevated serotonin levels during development, as other putative genetic risk factors for violence are also linked to an ontogenic excess of serotonin. I will outline a model whereby genetic predisposition to aggression – by altering structure and function within the socio-affective scaffold – amplifies the impact of early adverse life experience, creating stable sociocognitive biases which, in turn, lead to impulsive aggressive behavior. Finally, I will detail potential epigenetic mechanisms through which early adverse life experience might interact with genetic variation in MAOA to bring about the development of adult impulsive violence. 39
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<strong>EPFL</strong> <strong>Latsis</strong> <strong>Symposium</strong> <strong>2009</strong>: Understanding Violence<br />
S-13<br />
38<br />
February 11-13 <strong>2009</strong><br />
ge t t i n g t h e p h e n o t y p e s r i g h t : th e<br />
e s s e n t i a l i n g r e D i e n t t o u n D e r s t a n D i n g<br />
a e t i o l o g i c a l m e c h a n i s m s a n D D e v e l o p i n g<br />
e f f e c t i v e t r e a t m e n t s<br />
Hodgins, Sheilagh<br />
Institute of Psychiatry King’s College, University of London<br />
UK<br />
The population of individuals who as adults engage in persistent physical<br />
violence towards others is not homogeneous. The available evidence suggests<br />
that it includes at least three sub-groups. While all of the sub-groups<br />
display an early-onset pattern of antisocial behaviour that remains stable<br />
across the life-span, the sub-groups differ in behaviour, mental disorders,<br />
personality traits, emotion processing, cognitive abilities, attentional processes,<br />
and stress reactivity. These differences emerge at an early age and<br />
the sub-groups appear to remain distinct from childhood through adulthood.<br />
Yet, knowledge of the development of these sub-groups of individuals<br />
who become persistent violent offenders is very limited. Consequently,<br />
inadequate characterization of participants in investigations of genes that<br />
confer vulnerability for persistent violent behaviour, of brain structure and<br />
function, and in studies of the links between specific genes and brain structure<br />
and function limits the meaningfulness of the results. Accurate characterization<br />
of sub-groups of persistently violent individuals, at each developmental<br />
stage, is necessary in order to elucidate the complex mechanisms<br />
through the course of development that lead to an adult who persistently<br />
engages in violent behaviour towards others. Without understanding these<br />
developmental mechanisms, the establishment of effective prevention and<br />
treatment programmes is not likely.