Monoamine oxidase a gene promoter methylation and transcriptional downregulation in an offender population with antisocial personality disorder

  title={Monoamine oxidase a gene promoter methylation and transcriptional downregulation in an offender population with antisocial personality disorder},
  author={Dave Checknita and Gilles Maussion and Benoit Labont{\'e} and Stefano Comai and Richard E. Tremblay and Frank Vitaro and N Turecki and Antonella Bertazzo and Gabriella Gobbi and Gilles C{\^o}t{\'e} and Gustavo Turecki},
  journal={British Journal of Psychiatry},
  pages={216 - 222}
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… 
Monoamine Oxidase A in Antisocial Personality Disorder and Borderline Personality Disorder
Candidate gene studies have produced the most compelling evidence connecting MAO-A genetic variants to both ASPD and BPD, but conflicting results abound in the literature, making it highly unlikely that ASPD or BPD is related to a specific MAO -A genetic variant.
Monoamino Oxidase A Gene Single-Nucleotide Polymorphisms and Methylation Status and the Risk of Violent Suicide Attempts in Affective Disorder Patients
Female affective disorder patients with a history of violent suicide attempt were found to have a significantly increased frequency of the AA genotype in the rs5906957 single nucleotide polymorphism, and the MAOA gene exon I promoter region showed significantly decreased methylation in female violent suicide attempter(s).
Epigenetic signature of MAOA and MAOB genes in mental disorders
First evidence for MAOA methylation to be involved in treatment response prediction and as a potential mechanistic correlate of fear extinction is presented, and altered MAOA gene DNA methylation emerges as a possible pathogenetically relevant epigenetic mechanism in mental disorders.
Monoamine Oxidase A Hypomethylation in Obsessive-Compulsive Disorder: Reversibility By Successful Psychotherapy?
The present pilot data suggest MAOA hypomethylation as a potential risk marker of obsessive-compulsive disorder and an increase in MAOA methylation levels as a possible mechanistic correlate of response to cognitive behavioral therapy in obsessive-Compulsive disorder.
Associations of serotonin transporter gene promoter polymorphisms and monoamine oxidase A gene polymorphisms with oppositional defiant disorder in a Chinese Han population
The results suggest that 5-HTTLPR and MAOA-uVNTR gene variants may contribute to susceptibility to ODD.
Monoamine oxidase and agitation in psychiatric patients
Associations of monoamine oxidase A gene first exon methylation with sexual abuse and current depression in women
Hypermethylation of MAOA first exon mediated the association of SA with current depression, and both methylation levels and SA independently predicted lifetime depression.


Monoamine oxidase A (MAOA) and antisocial behaviors in the presence of childhood and adolescent maltreatment
  • B. Haberstick, J. Lessem, J. Hewitt
  • Psychology, Biology
    American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics
  • 2005
This work did not replicate a previous report that MAOA polymorphisms moderated the relationship between maltreatment and conduct problems, and there was, however, a non‐significant trend in the predicted direction.
Moderating role of the MAOA genotype in antisocial behaviour
The analyses revealed consistent evidence of G x E interactions, such that those with the low-activity MAOA variant who were exposed to adversity in childhood were significantly more likely to report offending in late adolescence and early adulthood.
MAOA, abuse exposure and antisocial behaviour: 30-year longitudinal study
Evidence is added that there is a stable G × E interaction involving MAOA, abuse exposure and antisocial behaviour across the life course, with those having the low-activity MAOA variant being significantly more likely to report later offending, conduct problems and hostility.
Evidence that the methylation state of the monoamine oxidase A (MAOA) gene predicts brain activity of MAO A enzyme in healthy men
The methylation status of the MAOA promoter (detected in white blood cells) can reliably predict the brain endophenotype, and the status of MAOA methylation observed in healthy males merits consideration as a variable contributing to interindividual differences in behavior.
Child maltreatment moderates the association of MAOA with symptoms of depression and antisocial personality disorder.
It is concluded that the Gene x Environment interplay at this locus (MAOA) contributes to both symptoms of ASPD and MD and that careful specification of child maltreatment may be essential if genetic association research is to produce replicable results.
Identification and characterization of putative methylation targets in the MAOA locus using bioinformatic approaches
A regulatory mechanism is proposed for the human MAOA according to which the MAOA expression in vivo is executed by the generation of tissue-specific transcripts initiated from the alternative promoters where transcriptional activation of a particular promoter is under epigenetic control.
Effects of Genotype and Child Abuse on DNA Methylation and Gene Expression at the Serotonin Transporter
Methylation effects on transcription may vary as a function of underlying gene motif and splice variant, and that the shore of CpG islands, upstream of TSS, may be of particular interest in examining environmental effects on methylation.
Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A.
Analytical results indicate that isolated complete MAOA deficiency in this family is associated with a recognizable behavioral phenotype that includes disturbed regulation of impulsive aggression.