Evidence map›Paper›PMID 26776902›Full record

ReviewProgress in neuro-psychopharmacology & biological psychiatry2016

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

Sean C Godar, Paula J Fite, Kenneth M McFarlin, Marco Bortolato

Abstract readReview
In one paragraph

Review in Progress in neuro-psychopharmacology & biological psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 110 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Sean C GodarDepartment of Pharmacology and Toxicology, University of Kansas, Lawrence, (KS), USA; Consortium for Translational Research on Aggression and Drug Abuse (ConTRADA), University of Kansas, Lawrence, (KS), USA.
Paula J FiteConsortium for Translational Research on Aggression and Drug Abuse (ConTRADA), University of Kansas, Lawrence, (KS), USA; Clinical Child Psychology Program, University of Kansas, Lawrence, (KS), USA.
Kenneth M McFarlinDepartment of Pharmacology and Toxicology, University of Kansas, Lawrence, (KS), USA; Consortium for Translational Research on Aggression and Drug Abuse (ConTRADA), University of Kansas, Lawrence, (KS), USA.
Marco BortolatoDepartment of Pharmacology and Toxicology, University of Kansas, Lawrence, (KS), USA; Consortium for Translational Research on Aggression and Drug Abuse (ConTRADA), University of Kansas, Lawrence, (KS), USA. Electronic address: bortolato@ku.edu.
University of Kansas · US

Funding

Deciphering gene-environment interactions in pathological reactive aggressionR01MH104603 · NIMH · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Marco Bortolato, Regina A. Mangieri · 2014 to 2026
$6.0M
NIMH NIH HHS R01 MH104603
6 · The paper itself

Abstract

Drawing upon the recent resurgence of biological criminology, several studies have highlighted a critical role for genetic factors in the ontogeny of antisocial and violent conduct. In particular, converging lines of evidence have documented that these maladaptive manifestations of aggression are influenced by monoamine oxidase A (MAOA), the enzyme that catalyzes the degradation of brain serotonin, norepinephrine and dopamine. The interest on the link between MAOA and aggression was originally sparked by Han Brunner's discovery of a syndrome characterized by marked antisocial behaviors in male carriers of a nonsense mutation of this gene. Subsequent studies showed that MAOA allelic variants associated with low enzyme activity moderate the impact of early-life maltreatment on aggression propensity. In spite of overwhelming evidence pointing to the relationship between MAOA and aggression, the neurobiological substrates of this link remain surprisingly elusive; very little is also known about the interventions that may reduce the severity of pathological aggression in genetically predisposed subjects. Animal models offer a unique experimental tool to investigate these issues; in particular, several lines of transgenic mice harboring total or partial loss-of-function Maoa mutations have been shown to recapitulate numerous psychological and neurofunctional endophenotypes observed in humans. This review summarizes the current knowledge on the link between MAOA and aggression; in particular, we will emphasize 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.

Indexed as

AggressionAnimalsBrainHumansMental DisordersMonoamine OxidaseMonoamine OxidaseAggressionAnimal modelsAntisocial behaviorMonoamine oxidase A

Identifiers

PMID26776902
PMCPMC4865459
OpenAlexW2222458118

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.