| dc.description.abstract | Antisocial personality disorder (ASPD) is a DSM-IV Axis II personality disorder with a prevalence of 3% and 1% in males and females respectively. Among the psychosocial traits associated with ASPD are anxiety, aggressive behavior, impulsivity as well as a dysfunctional planning and overall functioning within the social context. Imaging studies on subjects either with ASPD or displaying some of the main associated psychosocial traits, have shown significant abnormalities in volumetric measurements and activation, in several brain regions including the prefrontal cortex (PFC), orbitofrontal cortex (OFC), the temporal lobe and the amygdala-hippocampus complex. Abnormalities in the serotonergic pathway have often been found in subjects diagnosed with ASPD. Specific functional polymorphisms associated with reduced serotonergic activity including tryptophan (TPH) synthesis, serotonin (5-HT) reuptake into the presynaptic terminal regulated by the 5-HT transporter (5-HTT), and deamination of 5-HT by monoamine oxidase-A (MAOA), have been reported as precipitating factors, particularly in subjects with a history of exposure to stressful environments during their childhood. Exposure to adversity during childhood in and of itself, has been associated with an increased probability of developing ASPD. However, the molecular mechanisms through which chronic stress exerts its effect are largely unknown and have been studied, at best, within the context of other mental disorders like major depression disorder (MDD). Furthermore, examination of the role of stress and 5-HT interactions in the development and maintenance of ASPD as well as their potential mechanisms is for the most part absent. This review intends to give an overall image of the most consistent results that are relevant for the understanding of what the causes of ASPD may be, placing particular interest on two main modulating factors, stress and 5-HT. | |
