Abstract
While previous studies suggest that both genetic and environmental factors play an important role in the development of autism-related traits, little is known about potential biological mechanisms underlying these associations. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we examined prospective associations between DNA methylation (DNAm: nbirth = 804, nage 7 = 877) and trajectories of social communication deficits at age 8-17 years. Methylomic variation at three loci across the genome (false discovery rate = 0.048) differentiated children following high (n = 80) versus low (n = 724) trajectories of social communication deficits. This differential DNAm was specific to the neonatal period and not observed at 7 years of age. Associations between DNAm and trajectory membership remained robust after controlling for co-occurring mental health problems (i.e., hyperactivity/inattention, conduct problems). The three loci identified at birth were not replicated in the Generation R Study. However, to the best of our knowledge, ALSPAC is the only study to date that is prospective enough to examine DNAm in relation to longitudinal trajectories of social communication deficits from childhood to adolescence. Although the present findings might point to potentially novel sites that differentiate between a high versus low trajectory of social communication deficits, the results should be considered tentative until further replicated.
Highlights
Autism is associated with high health care utilization because of its persistence, long-term impairments, and high comorbidity with other psychiatric disorders (Ganz, 2007; Joshi et al, 2010; Simonoff et al, 2008)
Using longitudinal data spanning gestation to early adolescence, this study examined the extent to which genome-wide DNA methylation (DNAm) patterns prospectively associate with trajectories of social communication deficits
We highlight here three key findings: (a) three loci at birth were differently methylated between high and low trajectories of social communication deficits in a temporally specific way; (b) none of the loci identified at birth associated with known mQTLs or prenatal maternal risk exposure; (c) the observed links between DNAm and social communication deficits trajectories were not accounted for by co-occurring mental health problems
Summary
Autism is associated with high health care utilization because of its persistence, long-term impairments, and high comorbidity with other psychiatric disorders (Ganz, 2007; Joshi et al, 2010; Simonoff et al, 2008). It has been shown that autism has a strong heritable basis (64%–91%) (Tick, Bolton, Happe, Rutter, & Rijsdijk, 2016) and shares a common genetic vulnerability with other neuropsychiatric disorders such as attention-deficit/hyperactivity disorder (ADHD) (Lichtenstein, Carlstrom, Rastam, Gillberg, & Anckarsater, 2010). Environmental factors such as prenatal exposure to maternal smoking or stress play a role in the etiology of various neuropsychiatric disorders, including autism
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
