The Revised NEO Personality Inventory (NEO-PI-R, Costa and McCrae, 1992) has been used to derive a profile of antisocial personality disorder, confirmed by expert ratings ( Miller et al, 2001 Miller et al, 2005). MAOA- L has been associated with reduced aggression in older males ( Manuck et al, 2000), and is unrelated to antisocial behavior in schizophrenia ( Zammit et al, 2004). In adolescent females, MAOA- H (rather than MAOA- L) has been related to antisocial behavior in terms of alcohol problems ( Nilsson et al, 2008). MAOA-antisocial trait associations may vary with other sample characteristics.

The MAOA-environment interaction also confers risk for attention deficit which, in combination with conduct disorder, predicts antisocial personality disorder in adulthood ( Holmes et al, 2001). This interaction has been confirmed in meta-analyses, and is strongest in males ( Kim-Cohen et al, 2006 Taylor and Kim-Cohen, 2007). In the MAOA- L carriers, risk for conduct disorder and antisocial traits is enhanced by environmental stressors such as maltreatment ( Caspi et al, 2002 Foley et al, 2004 Huang et al, 2004 Nilsson et al, 2006). A small kindred study has linked MAOA deficiency, because of gene mutation, to impulsive aggression ( Brunner et al, 1993).

Low MAOA activity is implicated in antisocial behavior. The variable number of tandem repeats polymorphism (MAOA-uVNTR) of the MAOA gene on chromosome Xp11.23, produces genotypes with low (MAOA- L) and high (MAOA- H) activity ( Sabol et al, 1998 Huang et al, 2004). MAOA is a catabolic enzyme involved in regulating serotonin, noradrenalin, and dopamine ( Weyler et al, 1990). Here, we examined the effect of a functional polymorphism in the monoamine oxidase A ( MAOA) gene on emotional brain activity and antisocial traits. In the INTEGRATE model of brain organization, we consider how genetic variants may modulate brain systems for emotion, feeling and self regulation, and associated temperamental personality traits ( Williams et al, 2008 Williams and Gordon, 2007). Monoamines such as noradrenalin and serotonin may modulate these relationships, given that their metabolism varies according to MAOA variants, and that they modulate both emotional brain systems and antisocial aggression. The MAOA low activity variant may increase susceptibility to antisocial traits through alterations to the neural systems for processing threat-related emotion, especially for males.

Altered neural processing of anger in MAOA- L genotypes was localized to medial frontal, parietal, and superior temporo-occipital regions in males, but only to the superior occipital cortex in females. These traits were related to altered ERPs elicited 120–280ms post-stimulus, particularly for negative emotion. The MAOA- L genotype was distinguished by elevated scores on the index of antisocial traits. Genotype differences in ERPs were localized using LORETA. Participants underwent a brief assessment of personality traits and event-related potential (ERP) recording during an emotion-processing task. From an initial sample of 290 healthy participants, 210 had low (MAOA- L) or high (MAOA- H) activity variants. Here, we assessed the low (MAOA- L) activity variant in relation to both brain function and a behavioral index of antisocial traits. Association studies suggest that the low activity variant of the monoamine oxidase A (MAOA)-uVNTR polymorphism confers risk for emotional disturbances associated with antisocial traits, particularly in males.

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