Genetic and epigenetic associations of MAOA and NR3C1 with depression and childhood adversities
Open accessAbstract
Monoamine oxidase A (MAOA) harbours a polymorphic upstream variable-number tandem repeat (u-VNTR). The MAOA-L allele of the u-VNTR leads to decreased gene expression levels in vitro and has been found to increase the risk of conduct disorder in males with childhood adversities. Early-life adversities have been associated with hypermethylation of the glucocorticoid receptor (NR3C1). In this study, we first performed a genetic association analysis of the MAOA u-VNTR using individuals with depression (n = 392) and controls (n = 1276). Next, DNA methylation analyses of MAOA and NR3C1 were performed using saliva samples of depressed and control subgroups. Adult MAOA-L females with childhood adversities were found to have a higher risk of developing depression (p = 0.006) and overall MAOA methylation levels were decreased in depressed females compared to controls (mean depressed, 42% vs. mean controls, 44%; p = 0.04). One specific childhood adversity [early parental death (EPD)] was associated with hypermethylation of NR3C1 close to an NGFI-A binding site (mean EPD, 19% vs. mean non-EPD, 14%; p = 0.005). Regression analysis indicated that this association may be mediated by the MAOA-L allele (adjusted R2 = 0.24, ANOVA: F = 23.48, p < 0.001). Conclusively: (1) depression in females may result from a gene × childhood-adversity interaction and/or a dysregulated epigenetic programming of MAOA; (2) childhood-adversity subtypes may differentially impact DNA methylation at NR3C1; (3) baseline MAOA-genotypic variations may affect the extent of NR3C1 methylation.
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Overall methylation of MAOA was reduced in depressed patients.
“and the overall methylation of MAOA was reduced in depressed patients (130).”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [130]
The results section on MAOA hypomethylation in females with depression reports lower average methylation across the measured MAOA region in depressed women than in female controls (42% versus 44%; p = 0.04). The claim omits that the finding was limited to females and to a measured region spanning the first exon–intron junction, rather than MAOA methylation generally in all depressed patients. (LLM, conf=0.88)
Experimental — accuracy not yet measuredLower MAOA activity, associated with higher levels of relevant neurotransmitters, has been associated with increased risk of conduct disorder and antisocial behavior.
“Lower MAOA activity, which is associated with higher levels of the relevant neurotransmitters, has been associated with increased risk of conduct disorder and antisocial behavior (130, 131).”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [130]
The Introduction and ‘Increased risk of depression in MAOA-L females with childhood adversities’ section associate the low-transcription MAOA-L allele with conduct, aggressive and antisocial behaviour specifically in males exposed to childhood maltreatment. The same section describes increased neurotransmitter levels as probable, while Limitations says reduced expression has been established in vitro only. The claim omits those conditions and presents the neurotransmitter link more definitively than the paper does. (LLM, conf=0.87)
Experimental — accuracy not yet measuredCarriers of lower-MAOA-activity variants (higher risk alleles such as 3.5) of the 30 bp u-VNTR had higher risk of depression with histories of childhood trauma in females compared to those without trauma histories.
“carriers of the lower-MAOA-activity variants (i.e., the higher risk alleles such as 3.5) had a higher risk of depression with histories of childhood trauma in females compared to those who without trauma histories”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [130]
The MAOA-L gene × environment section reports increased depression risk among females with childhood adversities, and Fig. 1 compares MAOA-L females with and without adversities. The determination-of-repeats section identifies 3.5 repeats as the MAOA-L allele. However, the Statistical analyses section defines the female MAOA-L group as homozygous for that allele (L/L), not all carriers; heterozygous females were grouped with MAOA-H. (LLM, conf=0.87)
Experimental — accuracy not yet measuredA variant in the MAOA gene is associated with differential NR3C1 methylation.
“A variant in MAOA gene is associated with differential NR3C1 methylation (130).”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [130]
The section ‘Early parental death is associated with NR3C1 hypermethylation’ reports higher NR3C1 methylation among MAOA-L individuals with early parental death, but not among MAOA-L individuals without it. The claim omits that childhood-adversity condition and makes the association sound general. Page numbers are not provided in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredParental death was associated with hypermethylation of NR3C1 CpGs close to the NGFI-A binding site, in association with the L-allele (3.5 repeats) of the MAOA u-VNTR in salivary DNA samples.
“one specific type of childhood trauma (parental death) was associated with hypermethylation of the NR3C1 CpGs close to the NGFI-A binding site, at, in association with the L-allele (3.5 repeats) of the MAOA u-VNTR in salivary DNA samples (130).”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [130]
Lower-activity MAOA-allele (3.5 repeats) of the MAOA u-VNTR has been associated with NR3C1 hypermethylation after childhood trauma.
“the lower-activity MAOA-allele (3.5 repeats) of the MAOA u-VNTR has been associated with other epigenetic modifications, such as NR3C1 hypermethylation after childhood trauma (130).”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [130]
Some studies in this review have found evidence that some genotypic variation in some risk alleles can influence DNA methylation.
“Although some studies presented in this review have found evidence that some genotypic variation in some risk alleles can influence DNAm (Klengel et al., 2013; Melas et al., 2013; Perroud et al., 2016)”
From Can epigenetics shine a light on the biological pathways underlying major mental disorders? (2022) · cites this paper as Melas et al., 2013
Childhood parental loss was associated with increased methylation of the exon 1F NR3C1 gene promoter.
“In this study, and others132 childhood parental loss was associated with increased methylation of the exon 1F NR3C1 gene promoter”
From Early life adversity and the epigenetic programming of hypothalamic-pituitary-adrenal function (2014) · cites this paper as [132]
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“While studies in depression have found inconsistent DNAm changes (Domschke et al., 2015; Melas & Forsell, 2015; Melas et al., 2013); in candidate gene studies in anxiety disorders, the evidence points at a pattern of hypomethylation (Ziegler et al.”
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- Authors
- Melas, P. A., Wei, Y., Wong, C. C. Y., Sjöholm, L. K., Åberg, E., Mill, J., Schalling, M., Forsell, Y., & Lavebratt, C.
- Affiliations
- Karolinska University Hospital (SE)
- Department of Molecular Medicine and Surgery, Neurogenetics Unit, Karolinska Institutet, Stockholm, Sweden
- King's College London (GB)
- Karolinska Institutet (SE)
- Corresponding author
- Lavebratt, Catharina
- ORCID
- Venue
- International Journal of Neuropsychopharmacology
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-08-01
- Volume
- 16
- Issue
- 7
- Pages
- 1513-1528
- ISSN
- 1461-1457 (ISSN-L)
- 1469-5111
- OpenAlex
- W2008523946
- Cited by
- 220
- References
- 78
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 11 · 2023: 14 · 2022: 17 · 2021: 18 · 2020: 23 · 2019: 16 · 2018: 22 · 2017: 24 · 2016: 20 · 2015: 21 · 2014: 20 · 2013: 3
- FWCI
- 9.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The International Journal of Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Bodossaki Foundation
- Karolinska Institutet
- Stockholms Läns Landsting
- Vetenskapsrådet (2010-03631, 2008-03307, 2009-05546, 2011-04807)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- monoamine oxidase A, NR3C1, glucocorticoid receptor, DNA methylation, depression, childhood adversity, gene-environment interaction, epigenetic programming, sex differences
- MeSH terms
- Adult, Aged, Child, Depression, Environment, Female, Humans, Life Change Events, Male, Middle Aged, Monoamine Oxidase, Receptors, Glucocorticoid, Sex Factors, Chi-Square Distribution, Minisatellite Repeats, CpG Islands, DNA Methylation, Genetic Association Studies, Epigenomics
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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