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Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children
dc.contributor.authorSong, Ashley Y.
dc.contributor.authorBakulski, Kelly
dc.contributor.authorFeinberg, Jason I.
dc.contributor.authorNewschaffer, Craig
dc.contributor.authorCroen, Lisa A.
dc.contributor.authorHertz-Picciotto, Irva
dc.contributor.authorSchmidt, Rebecca J.
dc.contributor.authorFarzadegan, Homayoon
dc.contributor.authorLyall, Kristen
dc.contributor.authorFallin, M. Daniele
dc.contributor.authorVolk, Heather E.
dc.contributor.authorLadd-Acosta, Christine
dc.date.accessioned2022-12-05T16:40:46Z
dc.date.available2024-01-05 11:40:45en
dc.date.available2022-12-05T16:40:46Z
dc.date.issued2022-12
dc.identifier.citationSong, Ashley Y.; Bakulski, Kelly; Feinberg, Jason I.; Newschaffer, Craig; Croen, Lisa A.; Hertz-Picciotto, Irva ; Schmidt, Rebecca J.; Farzadegan, Homayoon; Lyall, Kristen; Fallin, M. Daniele; Volk, Heather E.; Ladd-Acosta, Christine (2022). "Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children." Autism Research 15(12): 2359-2370.
dc.identifier.issn1939-3792
dc.identifier.issn1939-3806
dc.identifier.urihttps://hdl.handle.net/2027.42/175224
dc.description.abstractParental age is a known risk factor for autism spectrum disorder (ASD), however, studies to identify the biologic changes underpinning this association are limited. In recent years, “epigenetic clock” algorithms have been developed to estimate biologic age and to evaluate how the epigenetic aging impacts health and disease. In this study, we examined the relationship between parental epigenetic aging and their child’s prospective risk of ASD and autism related quantitative traits in the Early Autism Risk Longitudinal Investigation study. Estimates of epigenetic age were computed using three robust clock algorithms and DNA methylation measures from the Infinium HumanMethylation450k platform for maternal blood and paternal blood specimens collected during pregnancy. Epigenetic age acceleration was defined as the residual of regressing chronological age on epigenetic age while accounting for cell type proportions. Multinomial logistic regression and linear regression models were completed adjusting for potential confounders for both maternal epigenetic age acceleration (n = 163) and paternal epigenetic age acceleration (n = 80). We found accelerated epigenetic aging in mothers estimated by Hannum’s clock was significantly associated with lower cognitive ability and function in offspring at 12 months, as measured by Mullen Scales of Early Learning scores (β = −1.66, 95% CI: −3.28, −0.04 for a one-unit increase). We also observed a marginal association between accelerated maternal epigenetic aging by Horvath’s clock and increased odds of ASD in offspring at 36 months of age (aOR = 1.12, 95% CI: 0.99, 1.26). By contrast, fathers accelerated aging was marginally associated with decreased ASD risk in their offspring (aOR = 0.83, 95% CI: 0.68, 1.01). Our findings suggest epigenetic aging could play a role in parental age risks on child brain development.Lay SummaryParental age is a risk factor for ASD; however, little is known about possible biologic aging changes that contribute to this association. We found that mothers with faster epigenetic aging and fathers with slower epigenetic aging, relative to their chronologic age, were at increased odds of having a child with ASD and/or decreased early learning, at 3 years of age. These findings suggest epigenetic aging in parents may play a role in neurodevelopment and ASD.
dc.publisherJohn Wiley & Sons, Inc.
dc.subject.otherepigenetic age
dc.subject.otherbiologic age
dc.subject.otherDNA methylation
dc.subject.otherparental age
dc.subject.otherage acceleration
dc.subject.otherautism-related traits
dc.subject.otherautism spectrum disorder
dc.titleAssociations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children
dc.typeArticle
dc.rights.robotsIndexNoFollow
dc.subject.hlbsecondlevelNeurosciences
dc.subject.hlbsecondlevelPsychology
dc.subject.hlbtoplevelHealth Sciences
dc.subject.hlbtoplevelSocial Sciences
dc.description.peerreviewedPeer Reviewed
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/175224/1/aur2822_am.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/175224/2/aur2822.pdf
dc.identifier.doi10.1002/aur.2822
dc.identifier.sourceAutism Research
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