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Book ChapterDOI

Neurobiological Mechanisms for Impulsive-Aggression: The Role of MAOA

TLDR
Current data on the genetics and neurobiology of individual differences in impulsive-aggression are reviewed, with particular attention to the role of genetic variation in Monoamine Oxidase A and its impact on serotonergic signaling within corticolimbic circuitry.
Abstract
Aggression may be present across a large part of the spectrum of psychopathology, and underlies costly criminal antisocial behaviors. Human aggression is a complex and underspecified construct, confounding scientific discovery. Nevertheless, some biologically tractable subtypes are apparent, and one in particular—impulsive (reactive) aggression—appears to account for many facets of aggression-related dysfunction in psychiatric illness. Impulsive-aggression is significantly heritable, suggesting genetic transmission. However, the specific neurobiological mechanisms that mediate genetic risk for impulsive-aggression remain unclear. Here, we review extant data on the genetics and neurobiology of individual differences in impulsive-aggression, with particular attention to the role of genetic variation in Monoamine Oxidase A (MAOA) and its impact on serotonergic signaling within corticolimbic circuitry.

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Citations
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selective Reductions in Prefrontal Glucose Metabolism in Murderers

TL;DR: The preliminary results suggest that deficits localized to the prefrontal cortex may be related to violence in a selected group of offenders, although further studies are needed to establish the generalizability of these findings to violent offenders in the community.

Genetic background of extreme violent behavior

TL;DR: In this article, the authors found that both low monoamine metabolism and neuronal membrane dysfunction are plausible factors in the etiology of extreme criminal violent behavior, and imply that at least about 5-10% of all severe violent crime in Finland is attributable to the aforementioned MAOA and CDH13 genotypes.
Journal ArticleDOI

Genetic background of extreme violent behavior.

TL;DR: Low monoamine metabolism and neuronal membrane dysfunction are indicated as plausible factors in the etiology of extreme criminal violent behavior, and imply that at least about 5–10% of all severe violent crime in Finland is attributable to the aforementioned MAOA and CDH13 genotypes.
Journal ArticleDOI

The role of monoamine oxidase A in aggression: Current translational developments and future challenges

TL;DR: How an integrated translational strategy coordinating clinical and preclinical research may prove critical to elucidate important aspects of the pathophysiology of aggression, and identify potential targets for its diagnosis, prevention and treatment is emphasized.
Journal ArticleDOI

Drugs related to monoamine oxidase activity.

TL;DR: Desirable effects of MAO inhibition include increased availability of monoamine neurotransmitters, decreased oxidative stress, decreased formation of neurotoxins, induction of pro-survival genes and antiapoptotic factors, and improved mitochondrial functions.
References
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Journal ArticleDOI

Selective reductions in prefrontal glucose metabolism in murderers

TL;DR: In this paper, the prefrontal cortex was found to have significantly lower glucose metabolism in both lateral and medial prefrontal cortex relative to controls, indicating a regional specificity for the prefrontal deficit in violent offenders.
Journal ArticleDOI

Some observations on cortical inputs to the macaque monkey amygdala: an anterograde tracing study.

TL;DR: Results from studies that have attempted to confirm the projections from several candidate afferent regions using 3H‐amino acid autoradiography as an anterograde tracer are reported.
Journal ArticleDOI

Abnormal neural responses to emotional visual stimuli in adolescents with conduct disorder

TL;DR: Functional magnetic resonance imaging during passive viewing of pictures with neutral or strong negative affective valence suggests an impairment of both the recognition of emotional stimuli and the cognitive control of emotional behavior in patients with CD, resulting in a propensity for aggressive behavior.
Journal ArticleDOI

MAOA and the neurogenetic architecture of human aggression.

TL;DR: This work proposes that the MAOA-L, by causing an ontogenic excess of 5-hydroxytryptamine, labilizes critical neural circuitry for social evaluation and emotion regulation (the 'socioaffective scaffold'), thereby amplifying the effects of adverse early-life experience and creating deleterious sociocognitive biases.
Journal ArticleDOI

Evidence for a dysfunctional prefrontal circuit in patients with an impulsive aggressive disorder

TL;DR: The behavioral performance of psychiatric patients with a disorder characterized by impulsive aggression, Intermittent Explosive Disorder, is measured and the link between dysfunction of the orbital/medial prefrontal circuit and impulsive aggressive behavior is extended.
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