An epigenome-wide association study in the case-control study to explore early development identifies differential DNA methylation near ZFP57 as associated with autistic traits / Ellen M. HOWERTON in Journal of Neurodevelopmental Disorders, 17 (2025)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 17 (2025) Titre : An epigenome-wide association study in the case-control study to explore early development identifies differential DNA methylation near ZFP57 as associated with autistic traits Type de document : texte imprimé Auteurs : Ellen M. HOWERTON, Auteur ; Valerie MORRILL, Auteur ; Rose SCHROTT, Auteur ; Jason DANIELS, Auteur ; Ashley Y. SONG, Auteur ; Kelly BENKE, Auteur ; Heather VOLK, Auteur ; Homayoon FARZADEGAN, Auteur ; Aimee ANIDO ALEXANDER, Auteur ; Amanda L. TAPIA, Auteur ; Gabriel S. DICHTER, Auteur ; Lisa A. CROEN, Auteur ; Lisa WIGGINS, Auteur ; Genevieve WOJCIK, Auteur ; M. Daniele FALLIN, Auteur ; Christine LADD-ACOSTA, Auteur Langues : Anglais (eng) Mots-clés : Humans  DNA Methylation/genetics  Male  Female  Case-Control Studies  Genome-Wide Association Study  Autism Spectrum Disorder/genetics  Child, Preschool  DNA-Binding Proteins/genetics  Transcription Factors/genetics  Epigenome  Quantitative Trait Loci  Repressor Proteins  Autism  DNA methylation  Quantitative trait  Social Responsiveness Scale  by the institutional review boards (IRBs) at each SEED site. SEED 1 recruitment  was approved by the IRB of each recruitment site: IRB-C, CDC Human Research  Protection Office  Kaiser Foundation Research Institute (KFRI) Kaiser Permanente  Northern California IRB, Colorado Multiple IRB, Emory University IRB, Georgia  Department of Public Health IRB, Maryland Department of Health and Mental Hygiene  IRB, Johns Hopkins Bloomberg School of Public Health IRB, University of North  Carolina IRB and Office of Human Research Ethics, IRB of The Children’s Hospital  of Philadelphia, and IRB of the University of Pennsylvania. All enrolled families  provided written consent for participation. Consent for publication: Not  applicable. Competing interests: CLA reports receiving consulting fees from the  University of Iowa for providing expertise on epigenetics outside of this work.  All other authors declare that they have no conflict of interest. The findings  and conclusions in this report are those of the authors and do not necessarily  represent the official position of the Centers for Disease Control and  Prevention. Index. décimale : PER Périodiques Résumé : BACKGROUND: Quantitative measures of autism spectrum disorder (ASD)-related traits can provide insight into trait presentation across the population. Previous studies have identified epigenomic variation associated with ASD diagnosis, but few have evaluated quantitative traits. We sought to identify DNA methylation patterns in child blood associated with Social Responsiveness Scale score, Second Edition (SRS). METHODS: We conducted an epigenome-wide association study of SRS in child blood at approximately age 5 in the Study to Explore Early Development, a case-control study of ASD in the United States. We measured DNA methylation using the Illumina 450K array with 857 samples in our analysis after quality control. We performed regression of the M-value to identify single sites or differentially methylated regions (DMRs) associated with SRS scores, adjusting for sources of biological and technical variation. We examined methylation quantitative trait loci and conducted gene-ontology-term pathway analyses for regions of interest. RESULTS: We identified a region about 3.5 kb upstream of ZFP57 on chromosome 6 as differentially methylated (family-wise error rate [fwer] < 0.1) by continuous SRS T-score in the full sample (N = 857; fwer = 0.074) and among ASD cases only (N = 390; fwer = 0.021). ZFP57 encodes a transcription factor involved in imprinting regulation and maintenance, and this DMR has been previously associated with ASD in brain and buccal samples. CONCLUSIONS: Blood DNA methylation near ZFP57 was associated (fwer < 0.1) with SRS in the full population sample and appears to be largely driven by trait heterogeneity within the autism case group. Our results indicate DNA methylation associations with ASD quantitative traits are observable in a population and provide insights into specific biologic changes related to autism trait heterogeneity. En ligne : https://dx.doi.org/10.1186/s11689-025-09637-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576 [article] An epigenome-wide association study in the case-control study to explore early development identifies differential DNA methylation near ZFP57 as associated with autistic traits [texte imprimé] / Ellen M. HOWERTON, Auteur ; Valerie MORRILL, Auteur ; Rose SCHROTT, Auteur ; Jason DANIELS, Auteur ; Ashley Y. SONG, Auteur ; Kelly BENKE, Auteur ; Heather VOLK, Auteur ; Homayoon FARZADEGAN, Auteur ; Aimee ANIDO ALEXANDER, Auteur ; Amanda L. TAPIA, Auteur ; Gabriel S. DICHTER, Auteur ; Lisa A. CROEN, Auteur ; Lisa WIGGINS, Auteur ; Genevieve WOJCIK, Auteur ; M. Daniele FALLIN, Auteur ; Christine LADD-ACOSTA, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 17 (2025) Mots-clés : Humans  DNA Methylation/genetics  Male  Female  Case-Control Studies  Genome-Wide Association Study  Autism Spectrum Disorder/genetics  Child, Preschool  DNA-Binding Proteins/genetics  Transcription Factors/genetics  Epigenome  Quantitative Trait Loci  Repressor Proteins  Autism  DNA methylation  Quantitative trait  Social Responsiveness Scale  by the institutional review boards (IRBs) at each SEED site. SEED 1 recruitment  was approved by the IRB of each recruitment site: IRB-C, CDC Human Research  Protection Office  Kaiser Foundation Research Institute (KFRI) Kaiser Permanente  Northern California IRB, Colorado Multiple IRB, Emory University IRB, Georgia  Department of Public Health IRB, Maryland Department of Health and Mental Hygiene  IRB, Johns Hopkins Bloomberg School of Public Health IRB, University of North  Carolina IRB and Office of Human Research Ethics, IRB of The Children’s Hospital  of Philadelphia, and IRB of the University of Pennsylvania. All enrolled families  provided written consent for participation. Consent for publication: Not  applicable. Competing interests: CLA reports receiving consulting fees from the  University of Iowa for providing expertise on epigenetics outside of this work.  All other authors declare that they have no conflict of interest. The findings  and conclusions in this report are those of the authors and do not necessarily  represent the official position of the Centers for Disease Control and  Prevention. Index. décimale : PER Périodiques Résumé : BACKGROUND: Quantitative measures of autism spectrum disorder (ASD)-related traits can provide insight into trait presentation across the population. Previous studies have identified epigenomic variation associated with ASD diagnosis, but few have evaluated quantitative traits. We sought to identify DNA methylation patterns in child blood associated with Social Responsiveness Scale score, Second Edition (SRS). METHODS: We conducted an epigenome-wide association study of SRS in child blood at approximately age 5 in the Study to Explore Early Development, a case-control study of ASD in the United States. We measured DNA methylation using the Illumina 450K array with 857 samples in our analysis after quality control. We performed regression of the M-value to identify single sites or differentially methylated regions (DMRs) associated with SRS scores, adjusting for sources of biological and technical variation. We examined methylation quantitative trait loci and conducted gene-ontology-term pathway analyses for regions of interest. RESULTS: We identified a region about 3.5 kb upstream of ZFP57 on chromosome 6 as differentially methylated (family-wise error rate [fwer] < 0.1) by continuous SRS T-score in the full sample (N = 857; fwer = 0.074) and among ASD cases only (N = 390; fwer = 0.021). ZFP57 encodes a transcription factor involved in imprinting regulation and maintenance, and this DMR has been previously associated with ASD in brain and buccal samples. CONCLUSIONS: Blood DNA methylation near ZFP57 was associated (fwer < 0.1) with SRS in the full population sample and appears to be largely driven by trait heterogeneity within the autism case group. Our results indicate DNA methylation associations with ASD quantitative traits are observable in a population and provide insights into specific biologic changes related to autism trait heterogeneity. En ligne : https://dx.doi.org/10.1186/s11689-025-09637-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576

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 Auteurs : Ashley Y. SONG, Auteur ; Kelly M. BAKULSKI, Auteur ; Jason I. FEINBERG, Auteur ; Craig J. 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 (ÃŽ2 = -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] / Ashley Y. SONG, Auteur ; Kelly M. BAKULSKI, Auteur ; Jason I. FEINBERG, Auteur ; Craig J. 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 (ÃŽ2 = -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

Prenatal exposure to pesticide residues in the diet in association with child autism-related traits: Results from the EARLI study / Emily E. JOYCE in Autism Research, 15-5 (May 2022)  

Public ISBD [article]  inAutism Research > 15-5 (May 2022) . - p.957-970 Titre : Prenatal exposure to pesticide residues in the diet in association with child autism-related traits: Results from the EARLI study Type de document : texte imprimé Auteurs : Emily E. JOYCE, Auteur ; Jorge E. CHAVARRO, Auteur ; Juliette RANDO, Auteur ; Ashley Y. SONG, Auteur ; Lisa A. CROEN, Auteur ; M. Daniele FALLIN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Heather E. VOLK, Auteur ; Craig J. NEWSCHAFFER, Auteur ; Kristen LYALL, Auteur Article en page(s) : p.957-970 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder  Autistic Disorder  Child  Child, Preschool  Diet  Female  Humans  Mothers  Pesticide Residues  Pesticides/adverse effects  Pregnancy  Prenatal Exposure Delayed Effects  autism-related traits  fruit  prenatal diet  vegetables Index. décimale : PER Périodiques Résumé : Prior work has suggested associations between prenatal exposure to several classes of pesticides and child autism spectrum disorder (ASD). We examined a previously developed pesticide residue burden score (PRBS) and intake of high pesticide residue foods in association with ASD-related traits. Participants were drawn from the Early Autism Risk Longitudinal Investigation (EARLI) (n = 256), a cohort following mothers who previously had a child with ASD through a subsequent pregnancy and that child's development. ASD-related traits were captured according to total Social Responsiveness Scale (SRS) scores at age 3 (mean raw total SRS score = 35.8). Dietary intake was assessed through a food frequency questionnaire collected during pregnancy. We also incorporated organic intake and fatty foods in modified versions of the PRBS. Associations between high-residue fruit and vegetable intake, the overall PRBS and modified versions of it, and SRS scores were assessed using multivariable linear regression. Overall, we did not observe associations between pesticide residues in foods and ASD-related outcomes, and modified versions of the PRBS yielded similar findings. However, reductions in ASD-related traits were observed with higher overall fruit and vegetable intake (adjusted estimates for Q4 vs. Q1: ? -12.76, 95%CI -27.8, 2.3). Thus, findings from this high familial probability cohort did not suggest relationships between pesticide residues in the diet according to the PRBS and ASD-related traits. Beneficial effects of fruit and vegetable intake may influence these relationships. Future work should consider fruit and vegetable intake in association with ASD-related outcomes. LAY SUMMARY: Diet is the main source of exposure to most pesticides in use today. In this study, we examined the relationship between pesticide exposure from residues in the diet during pregnancy and child autism-related traits. We found that these pesticide residues from the diet were not related to child autism-related outcomes at age three. However, higher prenatal fruit and vegetable intake was associated with reductions in child autism-related traits. En ligne : http://dx.doi.org/10.1002/aur.2698 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473 [article] Prenatal exposure to pesticide residues in the diet in association with child autism-related traits: Results from the EARLI study [texte imprimé] / Emily E. JOYCE, Auteur ; Jorge E. CHAVARRO, Auteur ; Juliette RANDO, Auteur ; Ashley Y. SONG, Auteur ; Lisa A. CROEN, Auteur ; M. Daniele FALLIN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Heather E. VOLK, Auteur ; Craig J. NEWSCHAFFER, Auteur ; Kristen LYALL, Auteur . - p.957-970. Langues : Anglais (eng) in Autism Research > 15-5 (May 2022) . - p.957-970 Mots-clés : Autism Spectrum Disorder  Autistic Disorder  Child  Child, Preschool  Diet  Female  Humans  Mothers  Pesticide Residues  Pesticides/adverse effects  Pregnancy  Prenatal Exposure Delayed Effects  autism-related traits  fruit  prenatal diet  vegetables Index. décimale : PER Périodiques Résumé : Prior work has suggested associations between prenatal exposure to several classes of pesticides and child autism spectrum disorder (ASD). We examined a previously developed pesticide residue burden score (PRBS) and intake of high pesticide residue foods in association with ASD-related traits. Participants were drawn from the Early Autism Risk Longitudinal Investigation (EARLI) (n = 256), a cohort following mothers who previously had a child with ASD through a subsequent pregnancy and that child's development. ASD-related traits were captured according to total Social Responsiveness Scale (SRS) scores at age 3 (mean raw total SRS score = 35.8). Dietary intake was assessed through a food frequency questionnaire collected during pregnancy. We also incorporated organic intake and fatty foods in modified versions of the PRBS. Associations between high-residue fruit and vegetable intake, the overall PRBS and modified versions of it, and SRS scores were assessed using multivariable linear regression. Overall, we did not observe associations between pesticide residues in foods and ASD-related outcomes, and modified versions of the PRBS yielded similar findings. However, reductions in ASD-related traits were observed with higher overall fruit and vegetable intake (adjusted estimates for Q4 vs. Q1: ? -12.76, 95%CI -27.8, 2.3). Thus, findings from this high familial probability cohort did not suggest relationships between pesticide residues in the diet according to the PRBS and ASD-related traits. Beneficial effects of fruit and vegetable intake may influence these relationships. Future work should consider fruit and vegetable intake in association with ASD-related outcomes. LAY SUMMARY: Diet is the main source of exposure to most pesticides in use today. In this study, we examined the relationship between pesticide exposure from residues in the diet during pregnancy and child autism-related traits. We found that these pesticide residues from the diet were not related to child autism-related outcomes at age three. However, higher prenatal fruit and vegetable intake was associated with reductions in child autism-related traits. En ligne : http://dx.doi.org/10.1002/aur.2698 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473

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