Antisocial personality disorder (
ASPD) often presents with highly impulsive, violent behavior, and pathological changes in the orbitofrontal cortex (OFC) and ventral striatum (VS) are implicated. Several compelling reasons support a relationship between low
monoamine oxidase-A (
MAO-A), an
enzyme that regulates
neurotransmitters, and
ASPD. These include
MAO-A knockout models in rodents evidencing impulsive aggression and positron emission tomography (PET) studies of healthy subjects reporting associations between low brain
MAO-A levels and greater impulsivity or aggression. However, a fundamental gap in the literature is that it is unknown whether brain
MAO-A levels are low in more severe, clinical disorders of impulsivity, such as
ASPD. To address this issue, we applied [(11)C]
harmine PET to measure
MAO-A total distribution volume (
MAO-A VT), an index of
MAO-A density, in 18 male
ASPD participants and 18 age- and sex-matched controls. OFC and VS
MAO-A VT were lower in
ASPD compared with controls (multivariate analysis of variance (MANOVA): F2,33=6.8, P=0.003; OFC and VS
MAO-A VT each lower by 19%). Similar effects were observed in other brain regions: prefrontal cortex, anterior cingulate cortex, dorsal putamen, thalamus, hippocampus, and midbrain (MANOVA: F7,28=2.7, P=0.029). In
ASPD, VS
MAO-A VT was consistently negatively correlated with self-report and behavioral measures of impulsivity (r=-0.50 to -0.52, all P-values<0.05). This study is the first to demonstrate lower brain
MAO-A levels in
ASPD. Our results support an important extension of preclinical models of impulsive aggression into a human disorder marked by pathological aggression and impulsivity.