Genetic architecture for human aggression: A study of gene–phenotype relationship in OMIM
Open accessAbstract
Genetic studies of human aggression have mainly focused on known candidate genes and pathways regulating serotonin and dopamine signaling and hormonal functions. These studies have taught us much about the genetics of human aggression, but no genetic locus has yet achieved genome‐significance. We here present a review based on a paradoxical hypothesis that studies of rare, functional genetic variations can lead to a better understanding of the molecular mechanisms underlying complex multifactorial disorders such as aggression. We examined all aggression phenotypes catalogued in Online Mendelian Inheritance in Man (OMIM), an Online Catalog of Human Genes and Genetic Disorders. We identified 95 human disorders that have documented aggressive symptoms in at least one individual with a well‐defined genetic variant. Altogether, we retrieved 86 causal genes. Although most of these genes had not been implicated in human aggression by previous studies, the most significantly enriched canonical pathways had been previously implicated in aggression (e.g., serotonin and dopamine signaling). Our findings provide strong evidence to support the causal role of these pathways in the pathogenesis of aggression. In addition, the novel genes and pathways we identified suggest additional mechanisms underlying the origins of human aggression. Genome‐wide association studies with very large samples will be needed to determine if common variants in these genes are risk factors for aggression. © 2015 Wiley Periodicals, Inc.
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Studies of rare human genetic conditions and gene knockouts in mice show that many genetic determinants play critical roles in shaping the emotional circuitry of the brain and modulating aggressive behavior.
“Studies of rare human genetic conditions [14] and gene knockouts (KOs) in mice [15, 16] show that many genetic determinants play critical roles in shaping the emotional circuitry of the brain and modulating aggressive behavior [17, 18].”
From An integrated analysis of genes and functional pathways for aggression in human and rodent models (2019) · cites this paper as [14]
Several recent reviews in human and animals have consistently identified these pathways.
“Indeed, several recent reviews in human and animals have consistently identified these pathways [11, 15, 51].”
From An integrated analysis of genes and functional pathways for aggression in human and rodent models (2019) · cites this paper as [51]
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- Authors
- Zhang‐James, Y., & Faraone, S. V.
- Affiliations
- SUNY Upstate Medical University (US)
- Corresponding author
- Faraone, Stephen V.
- Venue
- American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
- Publisher
- Wiley
- Published
- 2015-08-19
- Volume
- 171
- Issue
- 5
- Pages
- 641-649
- ISSN
- 1552-4841 (ISSN-L)
- 1552-485X
- OpenAlex
- W2144545031
- Cited by
- 48
- References
- 42
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 6 · 2023: 3 · 2021: 4 · 2020: 5 · 2019: 5 · 2018: 6 · 2017: 3 · 2016: 4 · 2015: 2
- FWCI
- 0.60
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal of Medical Genetics Part B Neuropsychiatric Genetics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (R01MH094469, R13MH059126)
- .G. Jebsen Centre for Research on Neuropsychiatric Disorders, University of Bergen, Bergen, Norway, the European Community's Seventh Framework Programme (FP7/2007-2013)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Social Sciences › Psychology › Clinical Psychology › Psychopathy, Forensic Psychiatry, Sexual Offending
- Keywords
- human aggression, genetic architecture, genotype-phenotype correlation, OMIM, rare variants, serotonin signaling, dopamine signaling, canonical pathways, complex diseases
- MeSH terms
- Aggression, Humans, Risk Factors, Genetic Variation, Genetic Predisposition to Disease, Databases, Genetic, Genome-Wide Association Study, Genetic Association Studies
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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