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dc.contributor.authorHannon, E
dc.contributor.authorSchendel, D
dc.contributor.authorLadd-Acosta, C
dc.contributor.authorGrove, J
dc.contributor.authorHansen, CS
dc.contributor.authorAndrews, SV
dc.contributor.authorHougaard, DM
dc.contributor.authorBresnahan, M
dc.contributor.authorMors, O
dc.contributor.authorHollegaard, MV
dc.contributor.authorBækvad-Hansen, M
dc.contributor.authorHornig, M
dc.contributor.authorMortensen, PB
dc.contributor.authorBørglum, AD
dc.contributor.authorWerge, T
dc.contributor.authorPedersen, MG
dc.contributor.authorNordentoft, M
dc.contributor.authorBuxbaum, J
dc.contributor.authorDaniele Fallin, M
dc.contributor.authorBybjerg-Grauholm, J
dc.contributor.authorReichenberg, A
dc.contributor.authorMill, J
dc.date.accessioned2018-04-05T10:59:02Z
dc.date.issued2018-03-28
dc.description.abstractAutism spectrum disorder (ASD) is a severe neurodevelopmental disorder characterized by deficits in social communication and restricted, repetitive behaviors, interests, or activities. The etiology of ASD involves both inherited and environmental risk factors, with epigenetic processes hypothesized as one mechanism by which both genetic and non-genetic variation influence gene regulation and pathogenesis. The aim of this study was to identify DNA methylation biomarkers of ASD detectable at birth.en_GB
dc.description.sponsorshipThis study was supported by grant HD073978 from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institute of Environmental Health Sciences, and National Institute of Neurological Disorders and Stroke; and by the Beatrice and Samuel A. Seaver Foundation. We acknowledge iPSYCH and The Lundbeck Foundation for providing samples and funding. The iPSYCH (The Lundbeck Foundation Initiative for Integrative Psychiatric Research) team acknowledges funding from The Lundbeck Foundation (grant numbers R102-A9118 and R155–2014-1724), the Stanley Medical Research Institute, the European Research Council (project number 294838), the Novo Nordisk Foundation for supporting the Danish National Biobank resource, and grants from Aarhus and Copenhagen Universities and University Hospitals, including support to the iSEQ Center, the GenomeDK HPC facility, and the CIRRAU Center. This research has been conducted using the Danish National Biobank resource, supported by the Novo Nordisk Foundation. JM is supported by funding from the UK Medical Research Council (MR/K013807/1) and a Distinguished Investigator Award from the Brain & Behavior Research Foundation. The SEED study was supported by Centers for Disease Control and Prevention (CDC) Cooperative Agreements announced under the RFAs 01086, 02199, DD11–002, DD06–003, DD04–001, and DD09–002 and the SEED DNA methylation measurements were supported by Autism Speaks Award #7659 to MDF. SA was supported by the Burroughs-Wellcome Trust training grant: Maryland, Genetics, Epidemiology and Medicine (MD-GEM). The SSC was supported by Simons Foundation (SFARI) award and NIH grant MH089606, both awarded to STW.en_GB
dc.identifier.citationVol. 10, pp. 19 -en_GB
dc.identifier.doi10.1186/s13073-018-0527-4
dc.identifier.urihttp://hdl.handle.net/10871/32324
dc.language.isoenen_GB
dc.publisherBioMed Centralen_GB
dc.rights© The Author(s). 2018. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.en_GB
dc.subjectAutismen_GB
dc.subjectDNA methylationen_GB
dc.subjectGeneticsen_GB
dc.subjectNeonatalen_GB
dc.subjectGenome-wide association study (GWAS)en_GB
dc.subjectEpigenome-wide association study (EWAS)en_GB
dc.subjectBirthen_GB
dc.subjectDNA methylation quantitative trait loci (mQTL)en_GB
dc.subjectPolygenic risk scoreen_GB
dc.subjectPrenatal smokingen_GB
dc.titleElevated polygenic burden for autism is associated with differential DNA methylation at birthen_GB
dc.typeArticleen_GB
dc.date.available2018-04-05T10:59:02Z
dc.identifier.issn1756-994X
dc.descriptionThis is the final version of the article. Available from BioMed Central via the DOI in this record.en_GB
dc.identifier.journalGenome Medicineen_GB


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