Understanding Genetic Risk for Aggression: Clues From the Brain’s Response to Social Exclusion

Eisenberger, Naomi I.; Way, Baldwin M.; Taylor, Shelley E.; Welch, William T.; Lieberman, Matthew D.

doi:10.1016/j.biopsych.2006.08.007

Cited by 194 publications

(154 citation statements)

References 32 publications

Supporting

Mentioning

139

Contrasting

Unclassified

Order By: Relevance

“…At first glance, these findings may appear inconsistent with our findings and the previous study showing dACC hyperactivation to social exclusion (Eisenberger et al, 2007). However, these prior results, combined with no resting state differences in glucose metabolism as a function of MAOA (Alia-Klein, , suggest a general dysfunction in the neural circuitry of cognitive-emotional control in people with the low-functioning allele.…”

Section: Discussioncontrasting

confidence: 99%

“…This study contributes to an emerging body of evidence suggesting that people at risk for reactive aggression show heightened brain reactivity in response to aversive interpersonal situations (Denson, in press;Eisenberger et al, 2007). Using the same provocation induction in the current research, another study found that dACC activation was greatest for men and women who were high in trait aggressiveness (Denson et al, 2009).…”

Section: Discussionsupporting

confidence: 57%

“…To our knowledge, only one study has examined the neural mechanisms underlying the relationship between MAOA genotype and responses to an emotionally aversive social situation (Eisenberger et al, 2007). In that fMRI study, healthy community residents were ignored during a ball-tossing game ostensibly played with two other participants.…”

Section: Discussionmentioning

confidence: 99%

“…One study found that among people with the MAOA-L genotype, the dACC was hyporeactive and the amygdala was hyperreactive when viewing angry and fearful faces (Meyer-Lindenberg et al, 2006). In contrast, another study found that after being excluded from a computer game, participants with the MAOA-L genotype showed dACC hyperactivation relative to participants with the MAOA-H genotype (Eisenberger, Way, Taylor, Welch, & Lieberman, 2007).…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

A Functional Polymorphism of the MAOA Gene Is Associated with Neural Responses to Induced Anger Control

Denson

Dobson‐Stone

Ronay³

et al. 2014

Journal of Cognitive Neuroscience

View full text Add to dashboard Cite

Abstract■ Aggressiveness is highly heritable. Recent experimental work has linked individual differences in a functional polymorphism of the monoamine oxidase-A gene (MAOA) to anger-driven aggression. Other work has implicated the dorsal ACC (dACC) in cognitive-emotional control and the amygdala in emotional arousal. The present imaging genetics study investigated dACC and amygdala reactivity to induced anger control as a function of MAOA genotype. A research assistant asked 38 healthy male undergraduates to control their anger in response to an insult by a rude experimenter. Men with the low-expression allele showed increased dACC and amygdala activation after the insult, but men with the high-expression allele did not. Both dACC and amygdala activation independently mediated the relationship between MAOA genotype and self-reported anger control. Moreover, following the insult, men with the high-functioning allele showed functional decoupling between the amygdala and dACC, but men with the low-functioning allele did not. These results suggest that heightened dACC and amygdala activation and their connectivity are neuroaffective mechanisms underlying anger control in participants with the low-functioning allele of the MAOA gene. ■

show abstract

Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

A Functional Polymorphism of the MAOA Gene Is Associated with Neural Responses to Induced Anger Control

Denson

Dobson‐Stone

Ronay³

et al. 2014

Journal of Cognitive Neuroscience

View full text Add to dashboard Cite

show abstract

“…Animal studies have identified genes that influence animal behavior, and human genome-wide association studies (GWASs) have linked certain neuropsychiatric diseases to interindividual differences in sequences of genes [1][2][3]. Moreover, certain common differences in genetic sequences were associated with human behavioral phenotypes such as anxiety [4], stress [5], and aggression [6]. However, although GWASs were able to associate several genetic differences in people with behavioral disorders and neuropsychiatric disease, the effects in most cases are small and explain only a small fraction of the interindividual variation in the population.…”

Section: Introductionmentioning

confidence: 99%

The dynamic epigenome and its implications for behavioral interventions: a role for epigenetics to inform disorder prevention and health promotion

Szyf

Tang

Hill

et al. 2016

Behav. Med. Pract. Policy Res.

View full text Add to dashboard Cite

The emerging field of behavioral epigenetics is producing a growing body of evidence that early life experience and social exposure can alter the way by which genes are marked with DNA methylation. We hypothesize that changes in DNA methylation as well as other epigenetic markers could generate stable phenotypes. Early life adversity appears to result in altered DNA methylation of genes in the brain and peripheral tissues, and these changes are associated with adverse phenotypic changes. Although the data are still sparse, early epigenetic studies have provided a proof of principle that experiences and the environment leave marks on genes, and thus suggest molecular and physical mechanisms for the epidemiological concept of gene-environment interaction. The main attraction of DNA methylation for type I (TI) translational prevention science is the fact that, different from genetic changes that are inherited from our ancestors, DNA methylation is potentially preventable and reversible and, therefore, there is a prospect of epigenetically targeted interventions. In addition, DNA methylation markers might provide an objective tool for assessing effects of early adverse experience on individual risks as well as providing objective measures of progress of an intervention. In spite of this great potential promise of the emerging field of social and translational epigenetics, many practical challenges remain that must be addressed before behavioral epigenetics could become translational epigenetics.

show abstract

Schizophrenia, Substance Abuse, and Violent Crime

Fazel

Långström²,

Hjern³

et al. 2009

JAMA

569

374

View full text Add to dashboard Cite

Context Persons with schizophrenia are thought to be at increased risk of committing violent crime 4 to 6 times the level of general population individuals without this disorder. However, risk estimates vary substantially across studies, and considerable uncertainty exists as to what mediates this elevated risk. Despite this uncertainty, current guidelines recommend that violence risk assessment should be conducted for all patients with schizophrenia. Objective To determine the risk of violent crime among patients diagnosed as having schizophrenia and the role of substance abuse in mediating this risk. Design, Setting, and Participants Longitudinal designs were used to link data from nationwide Swedish registers of hospital admissions and criminal convictions in 1973-2006. Risk of violent crime in patients after diagnosis of schizophrenia (n = 8003) was compared with that among general population controls (n = 80 025). Potential confounders (age, sex, income, and marital and immigrant status) and mediators (substance abuse comorbidity) were measured at baseline. To study familial confounding, we also investigated risk of violence among unaffected siblings (n = 8123) of patients with schizophrenia. Information on treatment was not available. Main Outcome Measure Violent crime (any criminal conviction for homicide, assault, robbery, arson, any sexual offense, illegal threats, or intimidation). Results In patients with schizophrenia, 1054 (13.2%) had at least 1 violent offense compared with 4276 (5.3%) of general population controls (adjusted odds ratio [OR], 2.0; 95% confidence interval [CI], 1.8-2.2). The risk was mostly confined to patients with substance abuse comorbidity (of whom 27.6% committed an offense), yielding an increased risk of violent crime among such patients (adjusted OR, 4.4; 95% CI, 3.9-5.0), whereas the risk increase was small in schizophrenia patients without substance abuse comorbidity (8.5% of whom had at least 1 violent offense; adjusted OR, 1.2; 95% CI, 1.1-1.4; P<.001 for interaction). The risk increase among those with substance abuse comorbidity was significantly less pronounced when unaffected siblings were used as controls (28.3% of those with schizophrenia had a violent offense compared with 17.9% of their unaffected siblings; adjusted OR, 1.8; 95% CI, 1.4-2.4; P<.001 for interaction), suggesting significant familial (genetic or early environmental) confounding of the association between schizophrenia and violence. Conclusions Schizophrenia was associated with an increased risk of violent crime in this longitudinal study. This association was attenuated by adjustment for substance abuse, suggesting a mediating effect. The role of risk assessment, management, and treatment in individuals with comorbidity needs further examination.

show abstract

Understanding Genetic Risk for Aggression: Clues From the Brain’s Response to Social Exclusion

Cited by 194 publications

References 32 publications

A Functional Polymorphism of the MAOA Gene Is Associated with Neural Responses to Induced Anger Control

A Functional Polymorphism of the MAOA Gene Is Associated with Neural Responses to Induced Anger Control

The dynamic epigenome and its implications for behavioral interventions: a role for epigenetics to inform disorder prevention and health promotion

Schizophrenia, Substance Abuse, and Violent Crime

Contact Info

Product

Resources

About