The role of monoamine oxidase A in the neurobiology of aggressive, antisocial, and violent behavior: A tale of mice and men
Open accessAbstract
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.
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The gene-environment interaction with early-life adversity and low MAOA activity/deficiency is prevalent in individuals diagnosed with antisocial personality disorder.
“The gene-environment interaction with early-life adversity and low enzymatic activity of MAOA, or MAOA deficiency, is prevalent within individuals diagnosed with antisocial personality disorder (see Kolla and Bortolato 2020).”
From Decoding the bidirectional links between alcohol misuse and aggression: toward a unified translational framework (2026) · cites this paper as Kolla and Bortolato 2020
The section on MAOA polymorphisms and environmental factors reports that childhood maltreatment combined with the MAOA-L variant predicted lifetime ASPD symptoms. It does not establish that this combination is prevalent among people diagnosed with ASPD, or equate the variant with MAOA deficiency. The paper also notes studies that failed to confirm the interaction; page numbers were unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe effects of genes on behavior may also be modified by sex-specific factors such as the levels of testosterone and Y-chromosome genes.
“the effects of genes on behavior may also be modified by sex-specific factors such as the levels of testosterone and Y-chromosome genes [140, 141].”
From Genetics of child aggression, a systematic review (2024) · cites this paper as [140]
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- Hare RD, 2003 Manual for the Revised Psychopathy Checklist (2nd ed.). Multi-Health Systems, Toronto, ON, Canada.
- Nemeroff CB, 2004 Early-Life Adversity, CRF Dysregulation, and Vulnerability to Mood and Anxiety Disorders. Psychopharmacol Bull. 38, 14– 20. 15278013
Cited by
Sorted by citations
Genetics of child aggression, a systematic review
Koyama, E., Kant, T., Takata, A., Kennedy, J. L., & Zai, C. C. (2024) · Translational Psychiatry · doi:10.1038/s41398-024-02870-7 · Cited by 33 · see citing works
The Cooperative Neuron: Cellular Foundations of Mental Life
Phillips, W. A. (2023) · doi:10.1093/oso/9780198876984.001.0001 · Cited by 13 · see citing works
Update on Antisocial Personality Disorder.
Black, D. W. (2024) · Current Psychiatry Reports · doi:10.1007/s11920-024-01528-x · Cited by 5 · see citing works
Russell, N. M., Frier, M. D., Bortolato, M., & Mangieri, R. A. (2026) · Psychopharmacology · doi:10.1007/s00213-025-06938-0 · Cited by 3 · see citing works
Self-citation
- Authors
- Kolla, N. J., & Bortolato, M.
- Affiliations
- Centre for Addiction and Mental Health (CA)
- University of Utah (US)
- Corresponding author
- Kolla, Nathan J.
- Bortolato, Marco
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2020-11
- Volume
- 194
- Pages
- 101875
- ISSN
- 0301-0082 (ISSN-L)
- PMC
- PMC7609507
- OpenAlex
- W3036818139
- Cited by
- 138
- References
- 400
- Citations by year
- 2026: 18 · 2025: 25 · 2024: 29 · 2023: 42 · 2022: 11 · 2021: 12 · 2020: 1
- FWCI
- 2.28
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Progress in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Social Sciences › Psychology › Clinical Psychology › Psychopathy, Forensic Psychiatry, Sexual Offending
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Keywords
- monoamine oxidase A, aggression, antisocial behavior, violent behavior, gene-environment interaction, child abuse, prenatal tobacco exposure, serotonin, catecholamines, neurobiology of aggression
- MeSH terms
- Aggression, Animals, Antisocial Personality Disorder, Behavior, Animal, Humans, Monoamine Oxidase, Social Behavior, Violence, Gene-Environment Interaction
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