Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children.
DNA methylation
age acceleration
autism spectrum disorder
autism-related traits
biologic age
epigenetic age
parental age
Journal
Autism research : official journal of the International Society for Autism Research
ISSN: 1939-3806
Titre abrégé: Autism Res
Pays: United States
ID NLM: 101461858
Informations de publication
Date de publication:
12 2022
12 2022
Historique:
received:
09
03
2022
accepted:
19
09
2022
pubmed:
4
10
2022
medline:
3
12
2022
entrez:
3
10
2022
Statut:
ppublish
Résumé
Parental 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.
Identifiants
pubmed: 36189953
doi: 10.1002/aur.2822
pmc: PMC9722613
mid: NIHMS1838117
doi:
Substances chimiques
Biological Products
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2359-2370Subventions
Organisme : NIEHS NIH HHS
ID : U24 ES028533
Pays : United States
Organisme : NICHD NIH HHS
ID : P50 HD103538
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES017646
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES023513
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES025574
Pays : United States
Organisme : NIEHS NIH HHS
ID : R24 ES030893
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES016443
Pays : United States
Organisme : Autism Speaks
Pays : United States
Organisme : NIEHS NIH HHS
ID : R24 ES028533
Pays : United States
Informations de copyright
© 2022 International Society for Autism Research and Wiley Periodicals LLC.
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