Psychopathology of antisocial personality disorder: from the structural, functional and biochemical perspectives

Abstract

Abstract Background Antisocial personality disorder (ASPD) is characterized by a lack of empathy, a sense of guiltlessness and shamelessness, as well as impulsiveness. ASPD is a relatively common psychiatric condition in the general population, whereas individuals with ASPD often have substantial social impairments and a lower quality of life, especially for those who have mental comorbidities. This review gives an overview of the etiological and clinical aspects of ASPD and critically examines ASPD from the structural, functional and biochemical perspectives. Results Twin and family studies showed genetic predisposition in ASPD. Some candidate genes associated with ASPD include SLC6A4, COMT, 5-HTR2A, TPH1, DRD2, OXTR, CACNG8, COL25A1 and several serotonergic genes. Environmental factors like adverse childhood experience (ACE) and active empathy deficits in toddlerhood play a role in the etiology of ASPD, whereas low intelligence or attainment, a large family size, a convicted parent, a disrupted family, and a young mother are predictors of antisocial personality. Structural abnormalities involving the corpus callosum, amygdala, putamen, anterior cingulate cortex, as well as orbitofrontal- and dorsolateral frontal cortices have been identified in ASPD. Other observed structural changes include a decrease in grey matter volume, whole-brain volume, and white matter volume and thickness. In addition, functional abnormalities involving autonomic activity, prefrontal functions, as well as brain functional networks like sensorimotor networks, cognitive networks and cortico-striatal connectivity have been reported. Biochemical factors associated with ASPD include fatty acid amide hydrolase (FAAH) reduction in the amygdala, as well as changes in plasma levels of inflammatory biomarkers and neurotropic factors [namely, tumor necrosis factor (TNF)-α, interleukin 10 (IL-10), transforming growth factor (TGF)-β1 and brain-derived neurotrophic factor (BNDF). Increased plasma levels of testosterone, ghrelin and cortisol and decreased levels of leptin have also been implicated in ASPD. Conclusions To date, there is no Food and Drug Administration (FDA) approved drugs for ASPD. Understanding the disease from different perspectives is important, as this provides insights into the underlying mechanisms of ASPD, whereas the associated biochemical markers can be used as potential diagnostic and treatment targets for ASPD.