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

Infant siblings and the investigation of autism risk factors / Craig J. NEWSCHAFFER in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.7 Titre : Infant siblings and the investigation of autism risk factors Type de document : texte imprimé Auteurs : Craig J. NEWSCHAFFER, Auteur ; Lisa A. CROEN, Auteur ; M. Daniele FALLIN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Danh V. NGUYEN, Auteur ; Nora L. LEE, Auteur ; Carmen A. BERRY, Auteur ; Homayoon FARZADEGAN, Auteur ; H. Nicole HESS, Auteur ; Rebecca LANDA, Auteur ; Susan E. LEVY, Auteur ; Maria L. MASSOLO, Auteur ; Stacey C. MEYERER, Auteur ; Sandra M. MOHAMMED, Auteur ; McKenzie C. OLIVER, Auteur ; Sally OZONOFF, Auteur ; Juhi PANDEY, Auteur ; Adam SCHROEDER, Auteur ; Kristine M. SHEDD-WISE, Auteur Article en page(s) : p.7 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Infant sibling studies have been at the vanguard of autism spectrum disorders (ASD) research over the past decade, providing important new knowledge about the earliest emerging signs of ASD and expanding our understanding of the developmental course of this complex disorder. Studies focused on siblings of children with ASD also have unrealized potential for contributing to ASD etiologic research. Moving targeted time of enrollment back from infancy toward conception creates tremendous opportunities for optimally studying risk factors and risk biomarkers during the pre-, peri- and neonatal periods. By doing so, a traditional sibling study, which already incorporates close developmental follow-up of at-risk infants through the third year of life, is essentially reconfigured as an enriched-risk pregnancy cohort study. This review considers the enriched-risk pregnancy cohort approach of studying infant siblings in the context of current thinking on ASD etiologic mechanisms. It then discusses the key features of this approach and provides a description of the design and implementation strategy of one major ASD enriched-risk pregnancy cohort study: the Early Autism Risk Longitudinal Investigation (EARLI). En ligne : http://dx.doi.org/10.1186/1866-1955-4-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Infant siblings and the investigation of autism risk factors [texte imprimé] / Craig J. NEWSCHAFFER, Auteur ; Lisa A. CROEN, Auteur ; M. Daniele FALLIN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Danh V. NGUYEN, Auteur ; Nora L. LEE, Auteur ; Carmen A. BERRY, Auteur ; Homayoon FARZADEGAN, Auteur ; H. Nicole HESS, Auteur ; Rebecca LANDA, Auteur ; Susan E. LEVY, Auteur ; Maria L. MASSOLO, Auteur ; Stacey C. MEYERER, Auteur ; Sandra M. MOHAMMED, Auteur ; McKenzie C. OLIVER, Auteur ; Sally OZONOFF, Auteur ; Juhi PANDEY, Auteur ; Adam SCHROEDER, Auteur ; Kristine M. SHEDD-WISE, Auteur . - p.7. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.7 Index. décimale : PER Périodiques Résumé : Infant sibling studies have been at the vanguard of autism spectrum disorders (ASD) research over the past decade, providing important new knowledge about the earliest emerging signs of ASD and expanding our understanding of the developmental course of this complex disorder. Studies focused on siblings of children with ASD also have unrealized potential for contributing to ASD etiologic research. Moving targeted time of enrollment back from infancy toward conception creates tremendous opportunities for optimally studying risk factors and risk biomarkers during the pre-, peri- and neonatal periods. By doing so, a traditional sibling study, which already incorporates close developmental follow-up of at-risk infants through the third year of life, is essentially reconfigured as an enriched-risk pregnancy cohort study. This review considers the enriched-risk pregnancy cohort approach of studying infant siblings in the context of current thinking on ASD etiologic mechanisms. It then discusses the key features of this approach and provides a description of the design and implementation strategy of one major ASD enriched-risk pregnancy cohort study: the Early Autism Risk Longitudinal Investigation (EARLI). En ligne : http://dx.doi.org/10.1186/1866-1955-4-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

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 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 H. RAHBAR, Auteur ; Andria RATCHFORD, Auteur ; Ann REYNOLDS, Auteur ; Steven A. 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] / 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 H. RAHBAR, Auteur ; Andria RATCHFORD, Auteur ; Ann REYNOLDS, Auteur ; Steven A. 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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