No evidence for interaction between <i>MAOA</i> and childhood adversity for antisocial behavior

Prichard, Zoë M.; Mackinnon, Andrew; Jorm, Anthony F; Easteal, Simon

doi:10.1002/ajmg.b.30581

Cited by 50 publications

(41 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A significant reduced risk for conduct disorder was found among short-allele carriers by Foley et al, when adjusted for childhood adversity and interaction effects (Foley et al 2004). However, several studies have failed to find any main effect of the MAOA-VNTR (Haberstick et al 2005;Nilsson et al 2006;Prichard et al 2008;Widom and Brzustowicz 2006;Young et al 2006). A meta-analysis confirmed the presence of interaction effects between the MAOA-VNTR and childhood maltreatment in relation to problem behavior among boys (Kim-Cohen et al 2006).…”

Section: Discussionmentioning

confidence: 87%

“…Since then, this finding has been replicated in at least four studies (Foley et al 2004;Kim-Cohen et al 2006;Nilsson et al 2006;Widom and Brzustowicz 2006). However, another study only found a non-significant trend in the same direction (Haberstick et al 2005), and in at least three further publications no significant interactions between childhood maltreatment and MAOA-VNTR in boys could be identified (Huizinga et al 2006;Prichard et al 2008;Young et al 2006). Our group previously reported that girls with the long (3.5 and 4 repeat) variant of the polymorphism are more likely to be involved in delinquent behavior in the presence of psychosocial risk ) and similar findings have recently been reported (PromWormley et al 2009).…”

Section: Introductionmentioning

confidence: 83%

See 1 more Smart Citation

Maltreatment, MAOA, and Delinquency: Sex Differences in Gene–Environment Interaction in a Large Population-Based Cohort of Adolescents

et al. 2010

View full text Add to dashboard Cite

The present study investigated a possible interaction between a functional polymorphism in the MAOA gene promoter (MAOA-VNTR) and childhood maltreatment in the prediction of adolescent male and female delinquency. A cohort of 1,825 high school students, 17-18 years old, completed an anonymous questionnaire during class hours which included questions on childhood maltreatment, sexual abuse, and delinquency. Saliva samples were collected for DNA isolation, and analyzed for the MAOA-VNTR polymorphism. Self-reported maltreatment was a strong risk factor for adolescent delinquent behavior. The MAOA genotype also showed a significant main effect when controlled for maltreatment. Boys with a short variant and girls with one or two long variants of the polymorphism showed a higher risk for delinquency when exposed to maltreatment. Our results confirm previous findings of an interaction between the MAOA-VNTR polymorphism and self-reported maltreatment. Results for boys and girls differ according to MAOA-VNTR genotype and direction of phenotypic expression.

show abstract

Section: Discussionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 83%

Maltreatment, MAOA, and Delinquency: Sex Differences in Gene–Environment Interaction in a Large Population-Based Cohort of Adolescents

et al. 2010

View full text Add to dashboard Cite

show abstract

“…For marker T102C (rs6313), the homozygous genotype CC showed an association with agitation and aggression in patients with Alzheimer disease (Lam et al 2004). However, Prichard et al (2008) failed to observe any significant association between this marker and a range of behaviors including psychosis, agitation, aberrant motor behavior, and depression. No association was found between rs6313 and suicidal behavior in normal subjects (Correa et al 2007), patients with schizophrenia (Ertugrul et al 2004), and suicide attempters (Zalsman et al 2005).…”

Section: Serotonin Receptorsmentioning

confidence: 85%

Genetic determinants of aggression and impulsivity in humans

Павлов¹,

2011

View full text Add to dashboard Cite

Human aggression/impulsivity-related traits have a complex background that is greatly influenced by genetic and non-genetic factors. The relationship between aggression and anxiety is regulated by highly conserved brain regions including amygdala, which controls neural circuits triggering defensive, aggressive, or avoidant behavioral models. The dysfunction of neural circuits responsible for emotional control was shown to represent an etiological factor of violent behavior. In addition to the amygdala, these circuits also involve the anterior cingulated cortex and regions of the prefrontal cortex. Excessive reactivity in the amygdala coupled with inadequate prefrontal regulation serves to increase the likelihood of aggressive behavior. Developmental alterations in prefrontal-subcortical circuitry as well as neuromodulatory and hormonal abnormality appear to play a role. Imbalance in testosterone/serotonin and testosterone/cortisol ratios (e.g., increased testosterone levels and reduced cortisol levels) increases the propensity toward aggression because of reduced activation of the neural circuitry of impulse control and self-regulation. Serotonin facilitates prefrontal inhibition, and thus insufficient serotonergic activity can enhance aggression. Genetic predisposition to aggression appears to be deeply affected by the polymorphic genetic variants of the serotoninergic system that influences serotonin levels in the central and peripheral nervous system, biological effects of this hormone, and rate of serotonin production, synaptic release and degradation. Among these variants, functional polymorphisms in the monoamine oxidase A (MAOA) and serotonin transporter (5-HTT) may be of particular importance due to the relationship between these polymorphic variants and anatomical changes in the limbic system of aggressive people. Furthermore, functional variants of MAOA and 5-HTT are capable of mediating the influence of environmental factors on aggression-related traits. In this review, we consider genetic determinants of human aggression, with special emphasis on genes involved in serotonin and dopamine metabolism and function.

show abstract

“…Most studies have focused on a single SNP providing a silent T102C polymorphism (rs6313) and have provided support for association with a range of behaviours, including psychosis, agitation, aberrant motor behaviour and depression (e.g. see Prichard et al 2008); however, these authors were unable to replicate a previous association reported for the CC genotype with agitation and aggression in Alzheimer's disease patients (Lam et al 2004). A second well-studied polymorphism is the G-1438A promoter SNP which is in nearly complete linkage disequilibrium with the silent T102C SNP has been examined in context of antisocial behaviours in alcohol dependents, and has been found to have signiWcant association with impulsive behaviour but not borderline or antisocial, personality disorders (Preuss et al 2001).…”

Section: Serotonin Receptorsmentioning

confidence: 99%

Genetics of human aggressive behaviour

2009

View full text Add to dashboard Cite

A consideration of the evolutionary, physiological and anthropological aspects of aggression suggests that individual differences in such behaviour will have important genetic as well as environmental underpinning. Surveys of the likely pathways controlling the physiological and neuronal processes involved highlight, as obvious targets to investigate, genes implicated in sexual differentiation, anxiety, stress response and the serotonin neurotransmitter pathway. To date, however, association studies on single candidates have provided little evidence for any such loci with a major effect size. This may be because genes do not operate independently, but function against a background in which other genetic and environmental factors are crucial. Indeed, a series of recent studies, particularly concentrating on the serotonin and norepinephrine metabolising enzyme, monoamine oxidase A, has emphasised the necessity of examining gene by environmental interactions if the contributions of individual loci are to be understood. These findings will have major significance for the interpretation and analysis of data from detailed whole genome association studies. Functional imaging studies of genetic variants affecting serotonin pathways have also provided valuable insights into potential links between genes, brain and aggressive behaviour.

show abstract

No evidence for interaction between MAOA and childhood adversity for antisocial behavior

Cited by 50 publications

References 24 publications

Maltreatment, MAOA, and Delinquency: Sex Differences in Gene–Environment Interaction in a Large Population-Based Cohort of Adolescents

Maltreatment, MAOA, and Delinquency: Sex Differences in Gene–Environment Interaction in a Large Population-Based Cohort of Adolescents

Genetic determinants of aggression and impulsivity in humans

Genetics of human aggressive behaviour

Contact Info

Product

Resources

About