Neonatal DNA methylation and early-onset conduct problems: A genome-wide, prospective study
Open accessAbstract
Early-onset conduct problems (CP) are a key predictor of adult criminality and poor mental health. While previous studies suggest that both genetic and environmental risks play an important role in the development of early-onset CP, little is known about potential biological processes underlying these associations. In this study, we examined prospective associations between DNA methylation (cord blood at birth) and trajectories of CP (4–13 years), using data drawn from the Avon Longitudinal Study of Parents and Children. Methylomic variation at seven loci across the genome (false discovery rate < 0.05) differentiated children who go on to develop early-onset (n = 174) versus low (n = 86) CP, including sites in the vicinity of the monoglyceride lipase (MGLL) gene (involved in endocannabinoid signaling and pain perception). Subthreshold associations in the vicinity of three candidate genes for CP (monoamine oxidase A [MAOA], brain-derived neurotrophic factor [BDNF], and FK506 binding protein 5 [FKBP5]) were also identified. Within the early-onset CP group, methylation levels of the identified sites did not distinguish children who will go on to persist versus desist in CP behavior over time. Overall, we found that several of the identified sites correlated with prenatal exposures, and none were linked to known genetic methylation quantitative trait loci. Findings contribute to a better understanding of epigenetic patterns associated with early-onset CP.
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In all cases, except for probe cg15384400, methylation of these sites was lower in the early-onset vs low CP groups.
“In all cases, except for probe cg15384400, methylation of these sites was lower in the early-onset vs low CP groups.”
From Genetics of child aggression, a systematic review (2024) · cites this paper as Cecil [127]
Seven differentially methylated sites (q-value < 0.05) were found between early-onset vs low CP groups.
“Seven differentially methylated sites (q-value < 0.05) between early-onset vs low CP groups”
From Genetics of child aggression, a systematic review (2024) · cites this paper as Cecil [127]
Three of the sites had genetic annotations: (i) cg02503763 in the promoter regulatory region of MGLL, a gene implicated in endocannabinoid signaling and nociperception; (ii) cg21579239, annotated to the 5'UTR region of TTBK2, a gene involved in tau protein phosphorylation, of which mutations have been linked to neurodegenerative disorders; and (iii) cg16006965 in the promoter regulatory region of
“Three of the sites had genetic annotations: (i) cg02503763in the promoter regulatory region of MGLL, a gene implicated in endocannabinoid signaling and nociperception ; (ii) cg21579239, annotated to the 5’UTR region of TTBK2, a gene involved in tau protein phosphorylation, of which mutations have been linked to neurodegenerative disorders; and (iii) cg16006965 in the promoter regulatory region of”
From Genetics of child aggression, a systematic review (2024) · cites this paper as Cecil [127]
The other four differentially methylated sites were distal to annotated transcripts: cg12628061 located between AK127270 (-407kb) and PPAP2B (-507kb), cg02131674 located closest to BASP1 (-123kb), cg15384400 located between ARAP2 (-12kb) and DTHD1 (+26 kb), and cg07128473 located between TRPS1 (-210kb) and EIF3H (+876 kb).
“The other four differentially methylated sites distal to annotated transcripts: cg12628061 located between AK127270 (-407kb) and PPAP2B (-507kb), cg02131674 located closest to BASP1 (-123kb), cg15384400 located between ARAP2 (-12kb) and DTHD1 ( + 26 kb), and cg07128473 located between TRPS1 (-210kb) and EIF3H ( + 876 kb).”
From Genetics of child aggression, a systematic review (2024) · cites this paper as Cecil [127]
Candidate genes included BDNF (cg01225698, cg18354203), FKBP5 (cg07061368) and the MAOA promoter region (i.e. TSS200; cg05443523).
“Candidate: BDNF (cg01225698, cg18354203), FKBP5 (cg07061368) and the MAOA promoter region (i.e. TSS200; cg05443523)”
From Genetics of child aggression, a systematic review (2024) · cites this paper as Cecil [127]
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Barker, E. D., Walton, E., & Cecil, C. A. M. (2018) · Journal of Child Psychology and Psychiatry · doi:10.1111/jcpp.12782 · Cited by 134 · see citing works
Self-citationEpigenetic signature of MAOA and MAOB genes in mental disorders
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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
- Authors
- Cecil, C. A. M., Walton, E., Jaffee, S. R., O'Connor, T., Maughan, B., Relton, C. L., Smith, R. G., McArdle, W., Gaunt, T. R., Ouellet-Morin, I., & Barker, E. D.
- Affiliations
- King's College London (GB)
- University of Bristol (GB)
- University of Pennsylvania (US)
- University of Exeter (GB)
- Corresponding author
- Cecil, Charlotte A. M.
- Barker, Edward D.
- ORCID
- Venue
- Development and Psychopathology
- Publisher
- Cambridge University Press (CUP)
- Published
- 2017-06-09
- Volume
- 30
- Issue
- 2
- Pages
- 383-397
- ISSN
- 0954-5794 (ISSN-L)
- 1469-2198
- PMC
- PMC7612607
- OpenAlex
- W2614018979
- Cited by
- 46
- References
- 97
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 8 · 2021: 8 · 2020: 6 · 2019: 8 · 2018: 5 · 2017: 1
- FWCI
- 6.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Development and Psychopathology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Explore Bristol Research (acceptedVersion, other-oa)
- Bristol Research (University of Bristol) (submittedVersion, other-oa)
- Research Portal (King's College London) (submittedVersion, other-oa)
- Funders
- Wellcome Trust (102215/2/13/2), 102215)
- University of Bristol (102215/2/13/2)
- Medical Research Council (102215, MC_UU_00011/4, 102215/2/13/2, MC_PC_15018)
- Biotechnology and Biological Sciences Research Council (BB/I025263/1)
- Economic and Social Research Council (ES/N001273/1, 102215/2/13/2)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD068437)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Psychopathy, Forensic Psychiatry, Sexual Offending
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Social Sciences › Psychology › Clinical Psychology › Child and Adolescent Psychosocial and Emotional Development
- Keywords
- early-onset conduct problems, DNA methylation, epigenetics, umbilical cord blood, monoglyceride lipase, monoamine oxidase A, brain-derived neurotrophic factor, FKBP5, endocannabinoid signaling, prenatal exposure, Avon Longitudinal Study of Parents and Children
- MeSH terms
- Adolescent, Child, Child, Preschool, Female, Fetal Blood, Humans, Infant, Newborn, Longitudinal Studies, Male, Age of Onset, DNA Methylation, Conduct Disorder, Epigenesis, Genetic, Genome-Wide Association Study
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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.
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