Exploring epistasis in candidate genes for antisocial personality disorder

Arias, Jorge Mauricio Cuartas; Acosta, Carlos Alberto Palacio; Valencia, Jenny García; Montoya, Gabriel; Viana, Juan Carlos Arango; Nieto, Omer Campo; Flórez, Andrés; Medellin, Beatriz E. Camarena; Montoya, Winston Rojas; Gutiérrez-Achury, Javier; Fuentes, Carlos Sabas Cruz; Berrío, Gabriel Bedoya; Ruiz-Linares, Andrés

doi:10.1097/ypg.0b013e3283437175

Cited by 25 publications

(11 citation statements)

References 72 publications

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“…Other researchers [18]–[21] have suggested that the serotonin system may be important in CU traits but we are aware of only two studies that have directly investigated the relationship between serotonergic function and CU traits. Fowler et al (2009) found that a variable number tandem repeat (VNTR) polymorphism in the gene encoding monoamine oxidase A (responsible for catabolism of serotonin and other catecholamine neurotransmitters), and an insertion/deletion polymorphism in the SLC6A4 promoter (5-HTTLPR) were associated with what the authors term the “emotional dysfunction” aspect of psychopathy (a construct that corresponds with CU traits) in a sample of adolescents with attention deficit hyperactivity disorder (ADHD) [18].…”

Section: Introductionmentioning

confidence: 98%

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An Exploration of the Serotonin System in Antisocial Boys with High Levels of Callous-Unemotional Traits

et al. 2013

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BackgroundThe serotonin system is thought to play a role in the aetiology of antisocial and aggressive behaviour in both adults and children however previous findings have been inconsistent. Recently, research has suggested that the function of the serotonin system may be specifically altered in a sub-set of antisocial populations – those with psychopathic (callous-unemotional) personality traits. We explored the relationships between callous-unemotional traits and functional polymorphisms of selected serotonin-system genes, and tested the association between callous-unemotional traits and serum serotonin levels independently of antisocial and aggressive behaviour.MethodParticipants were boys with antisocial behaviour problems aged 3–16 years referred to University of New South Wales Child Behaviour Research Clinics. Participants volunteered either a blood or saliva sample from which levels of serum serotonin (N = 66) and/or serotonin-system single nucleotide polymorphisms (N = 157) were assayed.ResultsFunctional single nucleotide polymorphisms from the serotonin 1b receptor gene (HTR1B) and 2a receptor gene (HTR2A) were found to be associated with callous-unemotional traits. Serum serotonin level was a significant predictor of callous-unemotional traits; levels were significantly lower in boys with high callous-unemotional traits than in boys with low callous-unemotional traits.Conclusion Results provide support to the emerging literature that argues for a genetically-driven system-wide alteration in serotonin function in the aetiology of callous-unemotional traits. The findings should be interpreted as preliminary and future research that aims to replicate and further investigate these results is required.

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Section: Introductionmentioning

confidence: 98%

“…Genes encoding the serotonin 2a receptor ( HTR2A ) and tryptophan hydroxylase 1 ( TPH1 ) have been associated with antisocial personality disorder (ASPD) in adult males [21]. Single nucleotide polymorphisms (SNPs) of the gene encoding the serotonin 1b receptor ( HTR1B ) have also been associated with anger and hostility [23].…”

Section: Introductionmentioning

confidence: 99%

An Exploration of the Serotonin System in Antisocial Boys with High Levels of Callous-Unemotional Traits

et al. 2013

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“…But they can also have unappreciated research consequences, particularly if psychiatric comorbidity varies systematically across different subgroups of smokers, but this heterogeneity is not taken into account. And if recent smokers increasingly deviate from their non-smoking counterparts genetically- either by virtue of greater psychiatric comorbidity or by having higher loadings on genetically-underpinned traits such as antisociality or impulsivity (Cuartas Arias et al, 2011; Pavlov et al, 2012), failure to systematically account for these differences could confound genetic analyses, or lead to identification of markers associated with comorbid diagnoses or traits rather than nicotine dependence. A Swedish twin study alluded to such an effect, reporting that heritability estimates for tobacco use among females increased several-fold across the first 50 years of the 20th century (Kendler et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Smoking and psychopathology increasingly associated in recent birth cohorts

Talati¹,

Wickramaratne²,

Keyes³

et al. 2013

Drug and Alcohol Dependence

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Background: In recent decades, smoking has become an increasingly non-normative behavior. Because deviant behaviors are associated with greater clinical and genetic risks, current-generation smokers may have greater concentrations of psychiatric comorbidity than previous generations. We examined this question empirically by testing whether associations between measures of smoking, psychiatric diagnoses, and riskassociated personality traits, increased across seven birth-cohorts of the 20th century. Method: 4,326 subjects from a cross-sectional NIMH control sample were categorized into one of seven groups based on birth (born before 1930, and 1930s-‘80s) and one of three smoking levels (lifetime dependent smoker, never dependent smoker, never smoker smoking and ND were assessed using the Fagerstrom Test for Nicotine Dependence; psychiatric diagnoses (drug and alcohol dependence, major depression, and generalized anxiety disorder) using the Composite International Diagnostic Interview-Short Form, and personality traits (neuroticism and extraversion) with the Eysenck Personality Questionnaire. Result: Lifetime prevalence of smoking decreased across the seven cohorts. Associations between smoking and drug dependence, generalized anxiety, and neuroticism, as well as total psychiatric comorbidity, were greater in more recent cohorts [smoking-by-cohort interaction: p<0.01], with greatest increases contributed by nicotine-dependent smokers. Smoking was also independently associated with alcohol dependence and depression, but these associations did not significantly vary across cohorts. Conclusions: More recent generations included fewer persons who smoked, but their smoking was associated with greater psychiatric morbidity. Failure to account for systematic variation in comorbidity across smoking cohorts may lead to unwanted heterogeneity in clinical, and possibly genetic, studies of nicotine dependence.

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“…Gene-gene interactions can also be expected to occur. [102] , [107] Given the complex interplay of neurotransmitters, the effects of genetic polymorphisms can be corrected or aggravated by other genetic polymorphisms [102] , [107] .…”

Section: Resultsmentioning

confidence: 99%

Neurobiological Correlates in Forensic Assessment: A Systematic Review

Gronde

Kempes

et al. 2014

PLoS ONE

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BackgroundWith the increased knowledge of biological risk factors, interest in including this information in forensic assessments is growing. Currently, forensic assessments are predominantly focused on psychosocial factors. A better understanding of the neurobiology of violent criminal behaviour and biological risk factors could improve forensic assessments.ObjectiveTo provide an overview of the current evidence about biological risk factors that predispose people to antisocial and violent behaviour, and determine its usefulness in forensic assessment.MethodsA systematic literature search was conducted using articles from PsycINFO, Embase and Pubmed published between 2000 and 2013.ResultsThis review shows that much research on the relationship between genetic predisposition and neurobiological alterations with aggression is performed on psychiatric patients or normal populations. However, the number of studies comparing offenders is limited. There is still a great need to understand how genetic and neurobiological alterations and/or deficits are related to violent behaviour, specifically criminality. Most studies focus on only one of the genetic or neurobiological fields related to antisocial and/or violent behaviour. To reliably correlate the findings of these fields, a standardization of methodology is urgently needed.ConclusionFindings from the current review suggest that violent aggression, like all forms of human behaviour, both develops under specific genetic and environmental conditions, and requires interplay between these conditions. Violence should be considered as the end product of a chain of life events, during which risks accumulate and potentially reinforce each other, displaying or triggering a specific situation. This systematic review did not find evidence of predispositions or neurobiological alterations that solely explain antisocial or violent behaviour. With better designed studies, more correlation between diverse fields, and more standardisation, it might be possible to elucidate underlying mechanisms. Thus, we advocate maintaining the current case-by-case differentiated approach to evidence-based forensic assessment.

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Exploring epistasis in candidate genes for antisocial personality disorder

Abstract: This study suggests that gene interactions between genetic variants in COMT, 5-HTR2A and tryptophan hydroxylase gene would be associated with ASPD and influence the dopamine rewards pathways and modulate serotonin levels in ASPD.

Cited by 25 publications

References 72 publications

An Exploration of the Serotonin System in Antisocial Boys with High Levels of Callous-Unemotional Traits

An Exploration of the Serotonin System in Antisocial Boys with High Levels of Callous-Unemotional Traits

Smoking and psychopathology increasingly associated in recent birth cohorts

Neurobiological Correlates in Forensic Assessment: A Systematic Review

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