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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

Do aggressive and non-aggressive antisocial behaviors in adolescents result from the same genetic and environmental effects?

TL;DR: A partial genetic overlap with a specific genetic effect contributing to the variance of aggressive ASB and a stronger genetic effect on aggression in females than in males is suggested.
Journal ArticleDOI

Comparison of regional serotonin levels and turnover in the brain of naturally high and low aggressive rats.

TL;DR: High and low aggressive rats did not differ with regard to5-HT or 5-HIAA levels, but high aggressive rats showed faster 5-HT turnover than lowaggressive rats, and the involvement of serotonin in rat intraspecies aggression is discussed.
Journal ArticleDOI

Tryptophan Deprivation: Effects on Mouse-killing and Reactivity in the Rat

TL;DR: Prior non-aggressive interactions with mice significantly reduced later incidence of mouse-killing following a 4-week tryptophan-poor diet, thus confirming the suppressant effect of prior familiarization with mice on elicitation of mouse -killing as a result of brain 5-HT depletion.
Journal ArticleDOI

Genetic susceptibility for individual cooperation preferences: the role of monoamine oxidase A gene (MAOA) in the voluntary provision of public goods.

TL;DR: It is shown that there is a significant association between individuals' behavior in a repeated public goods game and the promoter-region functional repeat polymorphism in the monoamine oxidase A gene (MAOA), and the results suggest that male carriers of the low activity alleles cooperate significantly less than those carrying the high activity allele.
Journal ArticleDOI

Neurochemical correlates of muricidal behavior in rats.

TL;DR: The results here presented indicate that complete abolition of brain serotoninergic control is just enough per se to induce muricidal activity, well beyond any pre-existing strain predisposition to kill mice or not.
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