Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children / Ashley Y. SONG in Autism Research, 15-12 (December 2022)  

Public ISBD [article]  inAutism Research > 15-12 (December 2022) . - p.2359-2370 Titre : Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children Type de document : Texte imprimé et/ou numérique Auteurs : Ashley Y. SONG, Auteur ; Kelly BAKULSKI, Auteur ; Jason I. FEINBERG, Auteur ; Craig NEWSCHAFFER, Auteur ; Lisa A. CROEN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Homayoon FARZADEGAN, Auteur ; Kristen LYALL, Auteur ; M Daniele FALLIN, Auteur ; Heather E. VOLK, Auteur ; Christine LADD-ACOSTA, Auteur Article en page(s) : p.2359-2370 Langues : Anglais (eng) Mots-clés : Child  Male  Pregnancy  Female  Humans  Autism Spectrum Disorder/epidemiology/genetics  Prospective Studies  Parents  Cognition  Biological Products  Epigenesis, Genetic  DNA methylation  age acceleration  autism spectrum disorder  autism-related traits  biologic age  epigenetic age  parental age Index. décimale : PER Périodiques 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 (Î2 = -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. En ligne : http://dx.doi.org/10.1002/aur.2822 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=488 [article] Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children [Texte imprimé et/ou numérique] / Ashley Y. SONG, Auteur ; Kelly BAKULSKI, Auteur ; Jason I. FEINBERG, Auteur ; Craig NEWSCHAFFER, Auteur ; Lisa A. CROEN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Homayoon FARZADEGAN, Auteur ; Kristen LYALL, Auteur ; M Daniele FALLIN, Auteur ; Heather E. VOLK, Auteur ; Christine LADD-ACOSTA, Auteur . - p.2359-2370. Langues : Anglais (eng) in Autism Research > 15-12 (December 2022) . - p.2359-2370 Mots-clés : Child  Male  Pregnancy  Female  Humans  Autism Spectrum Disorder/epidemiology/genetics  Prospective Studies  Parents  Cognition  Biological Products  Epigenesis, Genetic  DNA methylation  age acceleration  autism spectrum disorder  autism-related traits  biologic age  epigenetic age  parental age Index. décimale : PER Périodiques 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 (Î2 = -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. En ligne : http://dx.doi.org/10.1002/aur.2822 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=488

The Study to Explore Early Development (SEED): A Multisite Epidemiologic Study of Autism by the Centers for Autism and Developmental Disabilities Research and Epidemiology (CADDRE) Network / Diana SCHENDEL in Journal of Autism and Developmental Disorders, 42-10 (October 2012)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 42-10 (October 2012) . - p.2121-2140 Titre : The Study to Explore Early Development (SEED): A Multisite Epidemiologic Study of Autism by the Centers for Autism and Developmental Disabilities Research and Epidemiology (CADDRE) Network Type de document : Texte imprimé et/ou numérique Auteurs : Diana SCHENDEL, Auteur ; Carolyn G. DIGUISEPPI, Auteur ; Lisa A. CROEN, Auteur ; M. Daniele FALLIN, Auteur ; Phil REED, Auteur ; Laura A. SCHIEVE, Auteur ; Lisa D. WIGGINS, Auteur ; Julie L. DANIELS, Auteur ; Judith K. GRETHER, Auteur ; Susan E. LEVY, Auteur ; Lisa MILLER, Auteur ; Craig J. NEWSCHAFFER, Auteur ; Jennifer A. PINTO-MARTIN, Auteur ; Cordelia ROBINSON, Auteur ; Gayle C. WINDHAM, Auteur ; Aimee A. ALEXANDER, Auteur ; Arthur S. AYLSWORTH, Auteur ; Pilar BERNAL, Auteur ; Joseph D. BONNER, Auteur ; Lisa BLASKEY, Auteur ; Chyrise BRADLEY, Auteur ; Jack COLLINS, Auteur ; Casara J. FERRETTI, Auteur ; Homayoon FARZADEGAN, Auteur ; Ellen GIARELLI, Auteur ; Marques HARVEY, Auteur ; Susan HEPBURN, Auteur ; Matthew HERR, Auteur ; Kristina KAPARICH, Auteur ; Rebecca LANDA, Auteur ; Li-Ching LEE, Auteur ; Brooke LEVENSELLER, Auteur ; Stacey MEYERER, Auteur ; Mohammad Hossein RAHBAR, Auteur ; Andria RATCHFORD, Auteur ; Ann REYNOLDS, Auteur ; Steven ROSENBERG, Auteur ; Julie RUSYNIAK, Auteur ; Stuart K. SHAPIRA, Auteur ; Karen S. SMITH, Auteur ; Margaret SOUDERS, Auteur ; Patrick Aaron THOMPSON, Auteur ; Lisa YOUNG, Auteur ; Marshalyn YEARGIN-ALLSOPP, Auteur Année de publication : 2012 Article en page(s) : p.2121-2140 Langues : Anglais (eng) Mots-clés : Autism  Epidemiology  Study methods  Risk factors  Phenotype Index. décimale : PER Périodiques Résumé : The Study to Explore Early Development (SEED), a multisite investigation addressing knowledge gaps in autism phenotype and etiology, aims to: (1) characterize the autism behavioral phenotype and associated developmental, medical, and behavioral conditions and (2) investigate genetic and environmental risks with emphasis on immunologic, hormonal, gastrointestinal, and sociodemographic characteristics. SEED uses a case–control design with population-based ascertainment of children aged 2–5 years with an autism spectrum disorder (ASD) and children in two control groups—one from the general population and one with non-ASD developmental problems. Data from parent-completed questionnaires, interviews, clinical evaluations, biospecimen sampling, and medical record abstraction focus on the prenatal and early postnatal periods. SEED is a valuable resource for testing hypotheses regarding ASD characteristics and causes. En ligne : http://dx.doi.org/10.1007/s10803-012-1461-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=180 [article] The Study to Explore Early Development (SEED): A Multisite Epidemiologic Study of Autism by the Centers for Autism and Developmental Disabilities Research and Epidemiology (CADDRE) Network [Texte imprimé et/ou numérique] / Diana SCHENDEL, Auteur ; Carolyn G. DIGUISEPPI, Auteur ; Lisa A. CROEN, Auteur ; M. Daniele FALLIN, Auteur ; Phil REED, Auteur ; Laura A. SCHIEVE, Auteur ; Lisa D. WIGGINS, Auteur ; Julie L. DANIELS, Auteur ; Judith K. GRETHER, Auteur ; Susan E. LEVY, Auteur ; Lisa MILLER, Auteur ; Craig J. NEWSCHAFFER, Auteur ; Jennifer A. PINTO-MARTIN, Auteur ; Cordelia ROBINSON, Auteur ; Gayle C. WINDHAM, Auteur ; Aimee A. ALEXANDER, Auteur ; Arthur S. AYLSWORTH, Auteur ; Pilar BERNAL, Auteur ; Joseph D. BONNER, Auteur ; Lisa BLASKEY, Auteur ; Chyrise BRADLEY, Auteur ; Jack COLLINS, Auteur ; Casara J. FERRETTI, Auteur ; Homayoon FARZADEGAN, Auteur ; Ellen GIARELLI, Auteur ; Marques HARVEY, Auteur ; Susan HEPBURN, Auteur ; Matthew HERR, Auteur ; Kristina KAPARICH, Auteur ; Rebecca LANDA, Auteur ; Li-Ching LEE, Auteur ; Brooke LEVENSELLER, Auteur ; Stacey MEYERER, Auteur ; Mohammad Hossein RAHBAR, Auteur ; Andria RATCHFORD, Auteur ; Ann REYNOLDS, Auteur ; Steven ROSENBERG, Auteur ; Julie RUSYNIAK, Auteur ; Stuart K. SHAPIRA, Auteur ; Karen S. SMITH, Auteur ; Margaret SOUDERS, Auteur ; Patrick Aaron THOMPSON, Auteur ; Lisa YOUNG, Auteur ; Marshalyn YEARGIN-ALLSOPP, Auteur . - 2012 . - p.2121-2140. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 42-10 (October 2012) . - p.2121-2140 Mots-clés : Autism  Epidemiology  Study methods  Risk factors  Phenotype Index. décimale : PER Périodiques Résumé : The Study to Explore Early Development (SEED), a multisite investigation addressing knowledge gaps in autism phenotype and etiology, aims to: (1) characterize the autism behavioral phenotype and associated developmental, medical, and behavioral conditions and (2) investigate genetic and environmental risks with emphasis on immunologic, hormonal, gastrointestinal, and sociodemographic characteristics. SEED uses a case–control design with population-based ascertainment of children aged 2–5 years with an autism spectrum disorder (ASD) and children in two control groups—one from the general population and one with non-ASD developmental problems. Data from parent-completed questionnaires, interviews, clinical evaluations, biospecimen sampling, and medical record abstraction focus on the prenatal and early postnatal periods. SEED is a valuable resource for testing hypotheses regarding ASD characteristics and causes. En ligne : http://dx.doi.org/10.1007/s10803-012-1461-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=180

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