Evidence map›Paper›PMID 32574581›Full record

ReviewProgress in neurobiology2020

The role of monoamine oxidase A in the neurobiology of aggressive, antisocial, and violent behavior: A tale of mice and men.

Nathan J Kolla, Marco Bortolato

Abstract readReview
In one paragraph

Review in Progress in neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

45 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  4. Review
  5. Article
  6. Article
  7. Design, synthesis, and evaluation of 1, 3-dioxo-Journal of enzyme inhibition and medicinal chemistry · 2025
    Article
  8. Psychopathic Traits Associate With Later Schizophrenia.Acta psychiatrica Scandinavica · 2025
    Article
  9. Article
  10. Article
  11. Article
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  13. Sex-Dependent Effects ofJournal of child sexual abuse · 2025
    Article
  14. Article
  15. Article
  16. Biological Basis for the Formation of Suicidal Behavior: A Review.Medical journal of the Islamic Republic of Iran · 2025
    Review
  17. Article
  18. Article
  19. Review
  20. Update on Antisocial Personality Disorder.Current psychiatry reports · 2024
    Review
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

2 authors.

Nathan J KollaDepartment of Psychiatry, University of Toronto, Toronto, ON, Canada; Centre for Addiction and Mental Health (CAMH) Research Imaging Centre, Toronto, ON, Canada; Violence Prevention Neurobiological Research Unit, CAMH, Toronto, ON, Canada; Waypoint Centre for Mental Health Care, Penetanguishene, ON, Canada; Translational Initiative on Antisocial Personality Disorder (TrIAD); Program of Research on Violence Etiology, Neurobiology, and Treatment (PReVENT). Electronic address: nathan.kolla@camh.ca.
Marco BortolatoDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Utah, Salt Lake City, UT, USA; Translational Initiative on Antisocial Personality Disorder (TrIAD); Program of Research on Violence Etiology, Neurobiology, and Treatment (PReVENT). Electronic address: marco.bortolato@utah.edu.

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
CIHRNIMH NIH HHS R01 MH104603
6 · The paper itself

Abstract

Over the past two decades, research has revealed that genetic factors shape the propensity for aggressive, antisocial, and violent behavior. The best-documented gene implicated in aggression is MAOA (Monoamine oxidase A), which encodes the key enzyme for the degradation of serotonin and catecholamines. Congenital MAOA deficiency, as well as low-activity MAOA variants, has been associated with a higher risk for antisocial behavior (ASB) and violence, particularly in males with a history of child maltreatment. Indeed, the interplay between low MAOA genetic variants and early-life adversity is the best-documented gene × environment (G × E) interaction in the pathophysiology of aggression and ASB. Additional evidence indicates that low MAOA activity in the brain is strongly associated with a higher propensity for aggression; furthermore, MAOA inhibition may be one of the primary mechanisms whereby prenatal smoke exposure increases the risk of ASB. Complementary to these lines of evidence, mouse models of Maoa deficiency and G × E interactions exhibit striking similarities with clinical phenotypes, proving to be valuable tools to investigate the neurobiological mechanisms underlying antisocial and aggressive behavior. Here, we provide a comprehensive overview of the current state of the knowledge on the involvement of MAOA in aggression, as defined by preclinical and clinical evidence. In particular, we show how the convergence of human and animal research is proving helpful to our understanding of how MAOA influences antisocial and violent behavior and how it may assist in the development of preventative and therapeutic strategies for aggressive manifestations.

Indexed as

Antisocial Personality DisorderGene-Environment InteractionSocial BehaviorViolenceAggressionAnimalsBehavior, AnimalHumansMonoamine OxidaseMonoamine OxidaseAggressionAnimal modelsAntisocial personality disorderMonoamine oxidase APsychopathyViolence

Identifiers

PMID32574581
PMCPMC7609507

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Registered trials

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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.