Citation

Checknita D, Maussion G, Labonté B, Comai S, Tremblay RE, Vitaro F, Turecki N, Bertazzo A, Gobbi G, Côté G, Turecki G. Br. J. Psychiatry 2014; 206(3): 216-222.

Affiliation

D. Checknita, MSc, G. Maussion, PhD, McGill Group for Suicide Studies, Douglas Mental Health University Institute, McGill University, Montreal, Canada; B. Labonté, PhD, Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, USA; S. Comai, PhD, Neurobiological Psychiatry Unit, Department of Psychiatry, McGill University, Montreal, Canada; R. E. Tremblay, PhD, School of Public Health, Physiotherapy and Population Science, University College, Dublin, Ireland, and Departments of Pediatrics and Psychology, University of Montreal, Montreal, Canada; F. Vitaro, PhD, School of Psycho-Education, University of Montreal, Montreal, Canada; N. Turecki, McGill Group for Suicide Studies, Douglas Mental Health University Institute, McGill University, Montreal, Canada; A. Bertazzo, PhD, Department of Pharmaceutical Sciences, Univerity of Padua, Padua, Italy; G. Gobbi, MD, PhD, Neurobiological Psychiatry Unit, Department of Psychiatry, McGill University, Montreal, Canada; G. Côté, PhD, Institute Philippe-Pinel, Department of Psychology, Université de Québec à Trois-Rivères, Montreal, Canada; G. Turecki, MD, PhD, McGill Group for Suicide Studies, Douglas Mental Health University Institute, McGill University, Montreal, Canada.

Copyright

(Copyright © 2014, Royal College of Psychiatry)

DOI

10.1192/bjp.bp.114.144964

PMID

25497297

Abstract

Background Antisocial personality disorder (ASPD) is characterised by elevated impulsive aggression and increased risk for criminal behaviour and incarceration. Deficient activity of the monoamine oxidase A (MAOA) gene is suggested to contribute to serotonergic system dysregulation strongly associated with impulsive aggression and antisocial criminality. Aims To elucidate the role of epigenetic processes in altered MAOA expression and serotonin regulation in a population of incarcerated offenders with ASPD compared with a healthy non-incarcerated control population.

METHOD Participants were 86 incarcerated participants with ASPD and 73 healthy controls. MAOA promoter methylation was compared between case and control groups. We explored the functional impact of MAOA promoter methylation on gene expression in vitro and blood 5-HT levels in a subset of the case group.

RESULTS Results suggest that MAOA promoter hypermethylation is associated with ASPD and may contribute to downregulation of MAOA gene expression, as indicated by functional assays in vitro, and regression analysis with whole-blood serotonin levels in offenders with ASPD.

CONCLUSIONS These results are consistent with prior literature suggesting MAOA and serotonergic dysregulation in antisocial populations. Our results offer the first evidence suggesting epigenetic mechanisms may contribute to MAOA dysregulation in antisocial offenders.

Language: en