Genetics of aggressive behavior: An overview

Veroude, Kim; Zhang‐James, Yanli; Fernàndez‐Castillo, Noèlia; Bakker, Mireille J.; Cormand, Bru; Faraone, Stephen V.

doi:10.1002/ajmg.b.32364

Cited by 118 publications

(120 citation statements)

References 399 publications

(401 reference statements)

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“…Generally any action performed with the intention to harm another organism can be viewed as AGG [2, 3]. AGG is considered a common human behavior [4], with people varying in the degree of AGG they exhibit [5]. Children typically display AGG early in life, after which symptoms tend to diminish [6, 7], although in some individuals AGG persists into adulthood [8].…”

Section: Introductionmentioning

confidence: 99%

Genetic Association Study of Childhood Aggression across raters, instruments and age

Laan

Krapohl

et al. 2019

Preprint

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BackgroundHuman aggressive behavior (AGG) has a substantial genetic component. Here we present a large genome-wide association meta-analysis (GWAMA) of childhood AGG.MethodsWe analyzed assessments of AGG for a total of 328,935 observations from 87,485 children (aged 1.5 – 18 years), from multiple assessors, instruments, and ages, while accounting for sample overlap. We performed an overall analysis and meta-analyzed subsets of the data within rater, instrument, and age.ResultsHeritability based on the overall meta-analysis (AGGall) that could be attributed to Single Nucleotide Polymorphisms (SNPs) was 3.31% (SE=0.0038). No single SNP reached genome-wide significance, but gene-based analysis returned three significant genes: ST3GAL3 (P=1.6E-06), PCDH7 (P=2.0E-06) and IPO13 (P=2.5E-06). All three genes have previously been associated with educational traits. Polygenic scores based on our GWAMA significantly predicted aggression in a holdout sample of children and in retrospectively assessed childhood aggression. We obtained moderate-to-strong genetic correlations (rg‘s) with selected phenotypes from multiple domains, but hardly with any of the classical biomarkers thought to be associated with AGG. Significant genetic correlations were observed with most psychiatric and psychological traits (range |rg|: 0.19 –.1.00), except for obsessive-compulsive disorder. Aggression had a negative genetic correlation (rg =∼-0.5) with cognitive traits and age at first birth. Aggression was strongly genetically correlated with smoking phenotypes (range |rg|: 0.46 – 0.60). Genetic correlations between AGG and psychiatric disorders were strongest for mother- and self-reported AGG.ConclusionsThe current GWAMA of childhood aggression provides a powerful tool to interrogate the genetic etiology of AGG by creating individual polygenic scores and genetic correlations with psychiatric traits.

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Section: Introductionmentioning

confidence: 99%

Genetic Association Study of Childhood Aggression across raters, instruments and age

Laan

Krapohl

et al. 2019

Preprint

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“…Regarding the propensity to aggressive behavior, there are multiple factors interacting with each other. These factors include genetic [2–5] and environmental [6, 7] influences, as well as dysfunctional brain activity and/or anatomical brain damage, predominately localised to prefrontal and limbic structures [8, 9]. …”

Section: Introductionmentioning

confidence: 99%

Experimentally Assessed Reactive Aggression in Borderline Personality Disorder

et al. 2016

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Approximately 73% of patients suffering from Borderline personality disorder (BPD) exhibit aggressive behaviour, which severely hinders therapeutic work and clinical improvement. Because the underlying mechanisms of aggression in BPD are not yet completely understood, additional research in this domain has a high clinical and scientific relevance. We employed a modified version of the Taylor Aggression Paradigm (mTAP), in order to examine for the first time whether this task can be used to differentiate between BPD patients and healthy controls with regard to reactive aggression. In the mTAP, the amount of money subtracted by a virtual opponent was categorized into ‘low’ (10–20 cents) and ‘high’ (80–100 cents) provocations, enabling us to compare how much money BPD patients and healthy controls subtracted (i.e., how aggressively participants responded) following high and low provocation trials. Our results showed that, compared to healthy controls, BPD patients showed higher overall aggression, higher aggression after high provocation trials, as well as a larger difference between high and low provocation trials. This finding was corroborated by a neuropsychological assessment, demonstrating higher levels of aggression and impulsivity in BPD patients. Interestingly, reactive aggression in the mTAP was positively correlated with symptom severity and impulsivity in BPD patients. We suggest that the mTAP provides a valuable tool allowing psychiatrists to quantify reactive aggression in BPD. Therefore, clinicians and researchers might consider this task, as a short experimental measure of reactive aggression, either in future studies or to aid diagnostic assessment during clinical practice.

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“…This trait is a substantial cause of Neuropsychiatric Genetics mortality and morbidity globally [Anderson and Bushman, 2002;Veroude et al, 2015].…”

Section: Introductionmentioning

confidence: 99%

Comparative mRNA analysis of behavioral and genetic mouse models of aggression

Malki

Tosto

Pain

et al. 2016

American J of Med Genetics Pt B

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Mouse models of aggression have traditionally compared strains, most notably BALB/cJ and C57BL/6. However, these strains were not designed to study aggression despite differences in aggression-related traits and distinct reactivity to stress. This study evaluated expression of genes differentially regulated in a stress (behavioral) mouse model of aggression with those from a recent genetic mouse model aggression. The study used a discovery-replication design using two independent mRNA studies from mouse brain tissue. The discovery study identified strain (BALB/cJ and C57BL/6J) × stress (chronic mild stress or control) interactions. Probe sets differentially regulated in the discovery set were intersected with those uncovered in the replication study, which evaluated differences between high and low aggressive animals from three strains specifically bred to study aggression. Network analysis was conducted on overlapping genes uncovered across both studies. A significant overlap was found with the genetic mouse study sharing 1,916 probe sets with the stress model. Fifty-one probe sets were found to be strongly dysregulated across both studies mapping to 50 known genes. Network analysis revealed two plausible pathways including one centered on the UBC gene hub which encodes ubiquitin, a protein well-known for protein degradation, and another on P38 MAPK. Findings from this study support the stress model of aggression, which showed remarkable molecular overlap with a genetic model. The study uncovered a set of candidate genes including the Erg2 gene, which has previously been implicated in different psychopathologies. The gene networks uncovered points at a Redox pathway as potentially being implicated in aggressive related behaviors.

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Genetics of aggressive behavior: An overview

Cited by 118 publications

References 399 publications

Genetic Association Study of Childhood Aggression across raters, instruments and age

Genetic Association Study of Childhood Aggression across raters, instruments and age

Experimentally Assessed Reactive Aggression in Borderline Personality Disorder

Comparative mRNA analysis of behavioral and genetic mouse models of aggression

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