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Auteur Jason I. FEINBERG |
Documents disponibles écrits par cet auteur (2)
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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)
[article]
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
in Autism Research > 15-12 (December 2022) . - p.2359-2370[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 Association of Prenatal Vitamins and Folic Acid Supplement Intake with Odds of Autism Spectrum Disorder in a High-Risk Sibling Cohort, the Early Autism Risk Longitudinal Investigation (EARLI) / Katharine K. BRIEGER in Journal of Autism and Developmental Disorders, 52-6 (June 2022)
[article]
Titre : The Association of Prenatal Vitamins and Folic Acid Supplement Intake with Odds of Autism Spectrum Disorder in a High-Risk Sibling Cohort, the Early Autism Risk Longitudinal Investigation (EARLI) Type de document : Texte imprimé et/ou numérique Auteurs : Katharine K. BRIEGER, Auteur ; Kelly M. BAKULSKI, Auteur ; Celeste L. PEARCE, Auteur ; Ana BAYLIN, Auteur ; John F. DOU, Auteur ; Jason I. FEINBERG, Auteur ; Lisa A. CROEN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Craig J. NEWSCHAFFER, Auteur ; M Daniele FALLIN, Auteur ; Rebecca J. SCHMIDT, Auteur Article en page(s) : p.2801-2811 Langues : Anglais (eng) Mots-clés : Autism Folic acid Pregnancy cohort Prenatal vitamins Index. décimale : PER Périodiques Résumé : We examined maternal prenatal vitamin use or supplemental folic acid intake during month one of pregnancy for association with autism spectrum disorder (ASD) in the Early Autism Risk Longitudinal Investigation, an enriched-risk pregnancy cohort. Total folic acid intake was calculated from monthly prenatal vitamins, multivitamins, and other supplement reports. Clinical assessments through age 3 years classified children as ASD (n=38) or non-ASD (n=153). In pregnancy month one, prenatal vitamin use (59.7%) was not significantly associated with odds of ASD (OR=0.70, 95%CI 0.32, 1.53). Sample size was limited and residual confounding was possible. Given the estimated effect sizes in this and previous work, prenatal vitamin intake during early pregnancy could be a clinically useful preventative measure for ASD. En ligne : http://dx.doi.org/10.1007/s10803-021-05110-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=474
in Journal of Autism and Developmental Disorders > 52-6 (June 2022) . - p.2801-2811[article] The Association of Prenatal Vitamins and Folic Acid Supplement Intake with Odds of Autism Spectrum Disorder in a High-Risk Sibling Cohort, the Early Autism Risk Longitudinal Investigation (EARLI) [Texte imprimé et/ou numérique] / Katharine K. BRIEGER, Auteur ; Kelly M. BAKULSKI, Auteur ; Celeste L. PEARCE, Auteur ; Ana BAYLIN, Auteur ; John F. DOU, Auteur ; Jason I. FEINBERG, Auteur ; Lisa A. CROEN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Craig J. NEWSCHAFFER, Auteur ; M Daniele FALLIN, Auteur ; Rebecca J. SCHMIDT, Auteur . - p.2801-2811.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 52-6 (June 2022) . - p.2801-2811
Mots-clés : Autism Folic acid Pregnancy cohort Prenatal vitamins Index. décimale : PER Périodiques Résumé : We examined maternal prenatal vitamin use or supplemental folic acid intake during month one of pregnancy for association with autism spectrum disorder (ASD) in the Early Autism Risk Longitudinal Investigation, an enriched-risk pregnancy cohort. Total folic acid intake was calculated from monthly prenatal vitamins, multivitamins, and other supplement reports. Clinical assessments through age 3 years classified children as ASD (n=38) or non-ASD (n=153). In pregnancy month one, prenatal vitamin use (59.7%) was not significantly associated with odds of ASD (OR=0.70, 95%CI 0.32, 1.53). Sample size was limited and residual confounding was possible. Given the estimated effect sizes in this and previous work, prenatal vitamin intake during early pregnancy could be a clinically useful preventative measure for ASD. En ligne : http://dx.doi.org/10.1007/s10803-021-05110-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=474