Abstract
Violent offending is elevated among individuals with antisocial personality disorder (ASPD) and high psychopathic traits (PP). Morphological abnormalities of the amygdala and orbitofrontal cortex (OFC) are present in violent offenders, which may relate to the violence enacted by ASPD + PP. Among healthy males, monoamine oxidase-A (MAO-A) genetic variants linked to low in vitro transcription (MAOA-L) are associated with structural abnormalities of the amygdala and OFC. However, it is currently unknown whether amygdala and OFC morphology in ASPD relate to MAO-A genetic polymorphisms. We studied 18 ASPD males with a history of violent offending and 20 healthy male controls. Genomic DNA was extracted from peripheral leukocytes to determine MAO-A genetic polymorphisms. Subjects underwent a T1-weighted MRI anatomical brain scan that provided vertex-wise measures of amygdala shape and surface area and OFC cortical thickness. We found that ASPD + PP subjects with MAOA-L exhibited decreased surface area in the right basolateral amygdala nucleus and increased surface area in the right anterior cortical amygdaloid nucleus versus healthy MAOA-L carriers. This study is the first to describe genotype-related morphological differences of the amygdala in a population marked by high aggression. Deficits in emotional regulation that contribute to the violence of ASPD + PP may relate to morphological changes of the amygdala under genetic control.
Highlights
Antisocial personality disorder (ASPD), especially when high psychopathic traits are present (ASPD + PP), is associated with increased risk of violence[1]
Since MAOA-L shows a relationship with violent behavior and has been linked to amygdala/orbitofrontal cortex (OFC) structure, the principal aim of the study was to investigate whether the low-activity Monoamine oxidase-A (MAO-A) variant was associated with amygdala/OFC volume and morphology in antisocial personality disorder (ASPD) + PP with a history of violence
The plot shows that the sample size was sufficiently large enough to reliably detect the observed effects (Fig. 6). This investigation is the first to demonstrate that MAO-A variable nucleotide tandem repeat (VNTR) genetic polymorphisms show a relation with amygdala morphology in ASPD + PP
Summary
Antisocial personality disorder (ASPD), especially when high psychopathic traits are present (ASPD + PP), is associated with increased risk of violence[1]. The other study reported bilateral amygdala volume loss and atrophy of cortical, central, basolateral, and lateral nuclei that showed a relation with increased psychopathic traits in a predominantly male sample with high psychopathy features[12]. These studies highlight abnormal amygdala morphology as a potential biomarker of elevated psychopathic traits, but they do not provide information on possible genetic factors influencing this brain phenotype. A positron emission tomography investigation of ASPD found that MAO-A activity was lower in the OFC and regions that make direct connections with the amygdala, such as the hippocampus and thalamus[25]
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