Program & Abstract Book - EPFL Latsis Symposium 2009

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