Epigenomic strategies at the interface of genetic and environmental risk factors for autism
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Autism spectrum disorders (ASD) have been increasing in prevalence over the last two decades, primarily because of increased awareness and diagnosis. However, autism is clearly a complex human genetic disorder that involves interactions between genes and environment. Epigenetic mechanisms, such as DNA methylation, act at the interface of genetic and environmental risk and protective factors. Advancements in genome-wide sequencing has broadened the view of the human methylome and revealed the organization of the human genome into large-scale methylation domains that footprint over neurologically important genes involved in embryonic development. Future integrative epigenomic analyses of genetic risk factors with environmental exposures and methylome analyses are expected to be important for understanding the complex etiology of ASD.
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The establishment, maintenance, and removal of epigenetic marks are critical during neurodevelopment, and when disrupted can have significant impacts on neurodevelopment and cognitive function.
“The establishment, maintenance, and removal of epigenetic marks are critical during neurodevelopment and when disrupted can have significant impacts on neurodevelopment and cognitive function [ 63–66 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [65]
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Flagged first, then by citations
Research works printed but not linked: 2
- [63]Schmidt RJ Hansen RL Hartiala J Allayee H Schmidt LC Tancredi DJ Prenatal vitamins, functional one-carbon metabolism gene variants, and risk for autism in the CHARGE Study Epidemiology 2011 PMC3116691 21610500
- [112]Schroeder DI P L I K LaSalle JM Large-scale methylation domains mark a functional subset of neuronally expressed genes Genome Research 2011 in press PMC3202276 21784875
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Self-citation
- Authors
- LaSalle, J. M.
- Affiliations
- University of California, Davis (US)
- Corresponding author
- LaSalle, Janine M
- ORCID
- LaSalle, Janine M
- Venue
- Journal of Human Genetics
- Published
- 2013-05-16
- Volume
- 58
- Issue
- 7
- Pages
- 396-401
- ISSN
- 1434-5161 (ISSN-L)
- 1435-232X
- PMC
- PMC3955092
- OpenAlex
- W2021976298
- Cited by
- 95
- References
- 118
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 14 · 2021: 4 · 2020: 7 · 2019: 9 · 2018: 6 · 2017: 8 · 2016: 18 · 2015: 6 · 2014: 8 · 2013: 7
- FWCI
- 1.11
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Human Genetics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Defense (AR110194)
- International Rett Syndrome Foundation
- MIND Institute, University of California, Davis
- National Institutes of Health
- University of California, Davis
- National Institute of Neurological Disorders and Stroke (R01NS076263, R01NS081913)
- National Institute of Environmental Health Sciences (R01ES021707, P01ES011269, R21ES021330)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- autism spectrum disorder, epigenetics, DNA methylation, methylome, gene-environment interaction, genetic risk factors, environmental risk factors, embryonic development genes, autism etiology
- MeSH terms
- Autistic Disorder, Female, Humans, Infant, Newborn, Pregnancy, Risk Factors, Genome, Human, Perinatal Care, DNA Methylation, Genetic Predisposition to Disease, Epigenesis, Genetic, Genome-Wide Association Study, Epigenomics, Gene-Environment Interaction
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