scholarly journals Gene–environment interaction of monoamine oxidase A in relation to antisocial behaviour: current and future directions

2018 ◽  
Vol 125 (11) ◽  
pp. 1601-1626 ◽  
Author(s):  
Kent W. Nilsson ◽  
Cecilia Åslund ◽  
Erika Comasco ◽  
Lars Oreland
2006 ◽  
Vol 30 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Ann S. Masten

This article highlights the defining principles, progress and future directions in developmental psychopathology in relation to this special section. Six fundamental principles of developmental psychopathology are identified and the pervasive impact of this integrative framework on research, theory, and practice in behavioral health fields over the past three decades is described. This special section reflects the increasing influence of developmental systems theory, the growing focus on change, intensifying interest in translational research, and the increasingly complex and differentiated nature of research on pathways toward and away from psychopathology. A new era in developmental psychopathology is dawning, with exciting frontiers in brain development and plasticity, gene-environment interaction, resilience and recovery, multilevel dynamics, interdisciplinary research and training, and methodologies for assessing and analyzing change over time within and across individual systems and their contexts.


2007 ◽  
Vol 190 (1) ◽  
pp. 1-3 ◽  
Author(s):  
Anita Thapar ◽  
Kate Langley ◽  
Philip Asherson ◽  
Michael Gill

SummaryAttention-deficit hyperactivity disorder (ADHD) varies in its clinical presentation and course. Susceptibility gene variants for ADHD and associated antisocial behaviour are being identified with emerging evidence of gene–environment interaction. Genes and environmental factors that influence the origins of disorder are not necessarily the same as those that contribute to its course and outcome.


2017 ◽  
Vol 42 (4) ◽  
pp. 368-383 ◽  
Author(s):  
Stephen J. Watts ◽  
Melissa J. Tetzlaff-Bemiller ◽  
James C. McCutcheon

Involvement in drug markets is a significant risk factor for criminal victimization. Separately, the monoamine oxidase A (MAOA) gene has been identified as correlating with risky and antisocial behaviors and moderating the effects of environmental risk factors on antisocial behaviors. Using a sample drawn from the National Longitudinal Study of Adolescent to Adult Health ( N = 8,860), we explore whether MAOA genotype moderates the effect of drug selling on violent victimization. Results show that drug selling increases violent victimization among males, but not females. Additionally, the effect of drug selling on violent victimization among males is greater among the carriers of the 2R/3R alleles of MAOA, providing evidence of Gene × Environment interaction. These results appear despite a number of controls that potentially make the drug selling–violent victimization relationship spurious. Implications of the findings are discussed.


Author(s):  
Suzanne Vrshek-Schallhorn ◽  
Bradley M Avery ◽  
Vaibhav Sapuram

Gene–environment interaction (G×E) research in humans seeks to answer how specific genetic variation contributes to marked individual differences in responding to life experiences, primarily in regard to psychological functioning. In this chapter, we highlight theoretical models underlying G×E research, aspects of its history and controversies, the current state of G×E knowledge, and emerging and future directions for G×E research. Throughout this discussion, we show how this work has emerged across multiple units or levels of analyses, ranging from those closer to the biological functioning of the genes involved, such as neural activity in functional imaging, to more distal outcomes such as diagnoses of psychopathology. Important future directions for G×E research are transitioning from single variant to multiple variant approaches, and more carefully conceptualizing and measuring risk environments while also boosting sample sizes. Ultimately, by attending to these issues, G×E research can not only contribute to early detection of individuals with risky genetic and environmental profiles, but can also aid in revealing etiological pathways, thereby elucidating novel treatment approaches to mental illnesses.


2007 ◽  
Vol 19 (4) ◽  
pp. 1161-1180 ◽  
Author(s):  
Dante Cicchetti ◽  
Fred A. Rogosch ◽  
Melissa L. Sturge-Apple

AbstractChild maltreatment and polymorphisms of the serotonin transporter (5-HTT) and monoamine oxidase A (MAOA) genes were examined in relation to depressive symptomatology. Adolescents (Mage = 16.7 years) from low socioeconomic backgrounds with a history of child maltreatment (n= 207) or no such history (n= 132) were interviewed and provided buccal cells for genetic analysis. Gene × environment interactions were observed. Heightened depressive symptoms were found only among extensively maltreated youth with lowMAOAactivity. Among comparably maltreated youth with highMAOAactivity, self-coping strategies related to lower symptoms. Sexual abuse and the5-HTT short/shortgenotype predicted higher depression, anxiety, and somatic symptoms. This Gene × Environment interaction was further moderated byMAOAactivity level. The results highlight the protective functions of genetic polymorphisms and coping strategies in high risk youth and offer direction for understanding resilience and its promotion from a multiple levels of analysis perspective.


Children ◽  
2020 ◽  
Vol 7 (9) ◽  
pp. 122
Author(s):  
Meng-Che Tsai ◽  
Kai-Jyun Jhang ◽  
Chih-Ting Lee ◽  
Yu-Fang Lin ◽  
Carol Strong ◽  
...  

We aimed to investigate the effects of childhood adversity and its interaction with the polymorphisms in the monoamine oxidase A (MAOA), brain-derived neurotrophic factor (BDNF), and catechol-O-methyltransferase (COMT) genes on attention and hyperactivity disorder (ADHD) symptoms in a community sample of generally healthy youth. Participants (N = 432) completed questionnaires assessing ADHD symptoms (i.e., inattention, hyperactivity, and impulsiveness) and adverse childhood experiences, such as adverse environments (AEs) and childhood maltreatment (CM). Salivary genomic DNA was used to test polymorphisms in MAOA, BDNF, and COMT genes. A gene score (GS) was created based on the number of risk allele in the studied genes. Multiple linear regressions were used to examine the genetic and environmental effects on ADHD symptoms. The univariate analysis indicated that CM was significantly associated with inattention (β = 0.48 [95% confidence interval 0.16–0.79]), hyperactivity (0.25 [0.06–0.45]), and impulsiveness (1.16 [0.26–2.05]), while the GS was associated with hyperactivity (0.22 [0.11–0.33]) and impulsiveness (0.56 [0.06–1.05]). Only the GS remained significantly associated with hyperactivity (0.25 [0.12–0.37]) and impulsiveness (0.79 [0.20–1.38]) when the gene-environment interaction term was added in the model. No effects were found for AE and the gene-environment interaction term. In conclusion, CM was associated with ADHD symptoms in emerging adulthood. Genetic factors may also play a significant role in the association with these outcomes.


2008 ◽  
Vol 39 (4) ◽  
pp. 579-590 ◽  
Author(s):  
E. C. Prom-Wormley ◽  
L. J. Eaves ◽  
D. L. Foley ◽  
C. O. Gardner ◽  
K. J. Archer ◽  
...  

BackgroundRecent studies among males have reported a genotype–environment interaction (G×E) in which low-activity alleles at the monoamine oxidase A (MAOA) locus conferred greater sensitivity to the effects of childhood adversity on risk for conduct disorder (CD). So far, few studies of females have controlled for gene–environment correlation or used females heterozygous for this X-linked gene.MethodLogistic regression analysis of a sample of 721 females ages 8–17 years from the longitudinal Virginia Twin Study of Adolescent Behavioral Development (VTSABD) assessed the additive effects of MAOA genotypes on risk for CD, together with the main effect of childhood adversity and parental antisocial personality disorder (ASP), as well as the interaction of MAOA with childhood adversity on risk for CD.ResultsA significant main effect of genotype on risk for CD was detected, where low-activity MAOA imparted the greatest risk to CD in girls while controlling for the significant effects of maternal ASP and childhood adversity. Significant G×E with weak effect was detected when environmental exposure was untransformed, indicating a higher sensitivity to childhood adversity in the presence of the high-activity MAOA allele. The interaction was no longer statistically significant after applying a ridit transformation to reflect the sample sizes exposed at each level of childhood adversity.ConclusionsThe main effect of MAOA on risk for CD in females, its absence in males and directional difference of interaction is suggestive of genotype–sex interaction. As the effect of G×E on risk for CD was weak, its inclusion is not justified.


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