3-generation family histories of mental, neurologic, cardiometabolic, birth defect, asthma, allergy, and autoimmune conditions associated with autism: An open-source catalog of findings / Diana SCHENDEL in Autism Research, 17-10 (October 2024)  

Public ISBD [article]  inAutism Research > 17-10 (October 2024) . - p.2144-2155 Titre : 3-generation family histories of mental, neurologic, cardiometabolic, birth defect, asthma, allergy, and autoimmune conditions associated with autism: An open-source catalog of findings Type de document : texte imprimé Auteurs : Diana SCHENDEL, Auteur ; Linda EJLSKOV, Auteur ; Morten OVERGAARD, Auteur ; Zeal JINWALA, Auteur ; Viktor KIM, Auteur ; Erik T. PARNER, Auteur ; Amy E. KALKBRENNER, Auteur ; Christine LADD-ACOSTA, Auteur ; M. Daniele FALLIN, Auteur ; Sherlly XIE, Auteur ; Preben Bo MORTENSEN, Auteur ; Brian K. LEE, Auteur Article en page(s) : p.2144-2155 Langues : Anglais (eng) Mots-clés : allergy  asthma  autism  autoimmune  birth defect  cardiometabolic  family history  mental disorder  neurologic Index. décimale : PER Périodiques Résumé : Abstract The relatively few conditions and family member types (e.g., sibling, parent) considered in investigations of family health history in autism spectrum disorder (ASD, or autism) limits understanding of the role of family history in autism etiology. For more comprehensive understanding and hypothesis-generation, we produced an open-source catalog of autism associations with family histories of mental, neurologic, cardiometabolic, birth defect, asthma, allergy, and autoimmune conditions. All live births in Denmark, 1980 2012, of Denmark-born parents (1,697,231 births), and their 3-generation family members were followed through April 10, 2017 for each of 90 diagnoses (including autism), emigration or death. Adjusted hazard ratios (aHR) were estimated via Cox regression for each diagnosis-family member type combination, adjusting for birth year, sex, birth weight, gestational age, parental ages at birth, and number of family member types of index person; aHRs also calculated for sex-specific co-occurrence of each disorder. We obtained 6462 individual family history aHRS across autism overall (26,840 autistic persons; 1.6% of births), by sex, and considering intellectual disability (ID); and 350 individual co-occurrence aHRS. Results are cataloged in interactive heat maps and down-loadable data files: https://ncrr-au.shinyapps.io/asd-riskatlas/ and interactive graphic summaries: https://public.tableau.com/app/profile/diana.schendel/viz/ASDPlots_16918786403110/e-Figure5. While primarily for reference material or use in other studies (e.g., meta-analyses), results revealed considerable breadth and variation in magnitude of familial health history associations with autism by type of condition, family member type, sex of the family member, side of the family, sex of the index person, and ID status, indicative of diverse genetic, familial, and nongenetic autism etiologic pathways. Careful attention to sources of autism likelihood in family health history, aided by our open data resource, may accelerate understanding of factors underlying neurodiversity. En ligne : https://doi.org/10.1002/aur.3232 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=536 [article] 3-generation family histories of mental, neurologic, cardiometabolic, birth defect, asthma, allergy, and autoimmune conditions associated with autism: An open-source catalog of findings [texte imprimé] / Diana SCHENDEL, Auteur ; Linda EJLSKOV, Auteur ; Morten OVERGAARD, Auteur ; Zeal JINWALA, Auteur ; Viktor KIM, Auteur ; Erik T. PARNER, Auteur ; Amy E. KALKBRENNER, Auteur ; Christine LADD-ACOSTA, Auteur ; M. Daniele FALLIN, Auteur ; Sherlly XIE, Auteur ; Preben Bo MORTENSEN, Auteur ; Brian K. LEE, Auteur . - p.2144-2155. Langues : Anglais (eng) in Autism Research > 17-10 (October 2024) . - p.2144-2155 Mots-clés : allergy  asthma  autism  autoimmune  birth defect  cardiometabolic  family history  mental disorder  neurologic Index. décimale : PER Périodiques Résumé : Abstract The relatively few conditions and family member types (e.g., sibling, parent) considered in investigations of family health history in autism spectrum disorder (ASD, or autism) limits understanding of the role of family history in autism etiology. For more comprehensive understanding and hypothesis-generation, we produced an open-source catalog of autism associations with family histories of mental, neurologic, cardiometabolic, birth defect, asthma, allergy, and autoimmune conditions. All live births in Denmark, 1980 2012, of Denmark-born parents (1,697,231 births), and their 3-generation family members were followed through April 10, 2017 for each of 90 diagnoses (including autism), emigration or death. Adjusted hazard ratios (aHR) were estimated via Cox regression for each diagnosis-family member type combination, adjusting for birth year, sex, birth weight, gestational age, parental ages at birth, and number of family member types of index person; aHRs also calculated for sex-specific co-occurrence of each disorder. We obtained 6462 individual family history aHRS across autism overall (26,840 autistic persons; 1.6% of births), by sex, and considering intellectual disability (ID); and 350 individual co-occurrence aHRS. Results are cataloged in interactive heat maps and down-loadable data files: https://ncrr-au.shinyapps.io/asd-riskatlas/ and interactive graphic summaries: https://public.tableau.com/app/profile/diana.schendel/viz/ASDPlots_16918786403110/e-Figure5. While primarily for reference material or use in other studies (e.g., meta-analyses), results revealed considerable breadth and variation in magnitude of familial health history associations with autism by type of condition, family member type, sex of the family member, side of the family, sex of the index person, and ID status, indicative of diverse genetic, familial, and nongenetic autism etiologic pathways. Careful attention to sources of autism likelihood in family health history, aided by our open data resource, may accelerate understanding of factors underlying neurodiversity. En ligne : https://doi.org/10.1002/aur.3232 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=536

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

Autism spectrum disorder and birth spacing: Findings from the study to explore early development (SEED) / Laura A. SCHIEVE in Autism Research, 11-1 (January 2018)  

Public ISBD [article]  inAutism Research > 11-1 (January 2018) . - p.81-94 Titre : Autism spectrum disorder and birth spacing: Findings from the study to explore early development (SEED) Type de document : texte imprimé Auteurs : Laura A. SCHIEVE, Auteur ; Lin H. TIAN, Auteur ; Carolyn DREWS-BOTSCH, Auteur ; Gayle C. WINDHAM, Auteur ; Craig J. NEWSCHAFFER, Auteur ; Julie L. DANIELS, Auteur ; Li-Ching LEE, Auteur ; Lisa A. CROEN, Auteur ; M. Daniele FALLIN, Auteur Article en page(s) : p.81-94 Langues : Anglais (eng) Mots-clés : autism spectrum disorder  developmental disabilities  birth spacing  epidemiology  risk factor Index. décimale : PER Périodiques Résumé : Previous studies of autism spectrum disorder (ASD) and birth spacing had limitations; few examined phenotypic case subtypes or explored underlying mechanisms for associations and none assessed whether other (non ASD) developmental disabilities (DDs) were associated with birth spacing. We assessed associations between inter?pregnancy interval (IPI) and both ASD and other DDs using data from the Study to Explore Early Development, a multi?site case?control study with rigorous case?finding and case?classification methods and detailed data collection on maternal reproductive history. Our sample included 356 ASD cases, 627 DD cases, and 524 population (POP) controls born in second or later births. ASD and DD cases were further sub?divided according to whether the child had intellectual disability (ID). ASD cases were also sub?divided by ASD symptom severity, and DD cases were subdivided by presence of some ASD symptoms (indicated on an autism screener). Odds ratios, adjusted for maternal?child sociodemographic factors, (aORs) and 95% confidence intervals were derived from logistic regression models. Among term births, ASD was associated with both IPI <18 months (aOR 1.5 [1.1 2.2]) and ≥60 months (1.5 [0.99 2.4]). Both short and long IPI associations were stronger among ASD cases with high severity scores (aORs 2.0 [1.3 3.3] and 1.8 [0.99 3.2], respectively). Associations were unchanged after adding several factors potentially related to the causal pathway to regression models. DD was not associated with either short or long IPI?overall, among term births, or in any subgroup examined. These findings extend those from previous studies and further inform recommendations on optimal pregnancy spacing. Autism Res 2018, 11: 81 94. ? 2017 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary We investigated whether the amount of time between pregnancies was associated autism spectrum disorder (ASD) or other developmental disabilities (DD) in children. ASD was increased in second and later?born children who were conceived less than 18 months or 60 or more months after the mother's previous birth. Other DDs were not associated with birth spacing. En ligne : https://doi.org/10.1002/aur.1887 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=333 [article] Autism spectrum disorder and birth spacing: Findings from the study to explore early development (SEED) [texte imprimé] / Laura A. SCHIEVE, Auteur ; Lin H. TIAN, Auteur ; Carolyn DREWS-BOTSCH, Auteur ; Gayle C. WINDHAM, Auteur ; Craig J. NEWSCHAFFER, Auteur ; Julie L. DANIELS, Auteur ; Li-Ching LEE, Auteur ; Lisa A. CROEN, Auteur ; M. Daniele FALLIN, Auteur . - p.81-94. Langues : Anglais (eng) in Autism Research > 11-1 (January 2018) . - p.81-94 Mots-clés : autism spectrum disorder  developmental disabilities  birth spacing  epidemiology  risk factor Index. décimale : PER Périodiques Résumé : Previous studies of autism spectrum disorder (ASD) and birth spacing had limitations; few examined phenotypic case subtypes or explored underlying mechanisms for associations and none assessed whether other (non ASD) developmental disabilities (DDs) were associated with birth spacing. We assessed associations between inter?pregnancy interval (IPI) and both ASD and other DDs using data from the Study to Explore Early Development, a multi?site case?control study with rigorous case?finding and case?classification methods and detailed data collection on maternal reproductive history. Our sample included 356 ASD cases, 627 DD cases, and 524 population (POP) controls born in second or later births. ASD and DD cases were further sub?divided according to whether the child had intellectual disability (ID). ASD cases were also sub?divided by ASD symptom severity, and DD cases were subdivided by presence of some ASD symptoms (indicated on an autism screener). Odds ratios, adjusted for maternal?child sociodemographic factors, (aORs) and 95% confidence intervals were derived from logistic regression models. Among term births, ASD was associated with both IPI <18 months (aOR 1.5 [1.1 2.2]) and ≥60 months (1.5 [0.99 2.4]). Both short and long IPI associations were stronger among ASD cases with high severity scores (aORs 2.0 [1.3 3.3] and 1.8 [0.99 3.2], respectively). Associations were unchanged after adding several factors potentially related to the causal pathway to regression models. DD was not associated with either short or long IPI?overall, among term births, or in any subgroup examined. These findings extend those from previous studies and further inform recommendations on optimal pregnancy spacing. Autism Res 2018, 11: 81 94. ? 2017 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary We investigated whether the amount of time between pregnancies was associated autism spectrum disorder (ASD) or other developmental disabilities (DD) in children. ASD was increased in second and later?born children who were conceived less than 18 months or 60 or more months after the mother's previous birth. Other DDs were not associated with birth spacing. En ligne : https://doi.org/10.1002/aur.1887 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=333

Case-control meta-analysis of blood DNA methylation and autism spectrum disorder / Shan V. ANDREWS in Molecular Autism, 9 (2018)  

Public ISBD [article]  inMolecular Autism > 9 (2018) . - 40p. Titre : Case-control meta-analysis of blood DNA methylation and autism spectrum disorder Type de document : texte imprimé Auteurs : Shan V. ANDREWS, Auteur ; Brooke SHEPPARD, Auteur ; Gayle C. WINDHAM, Auteur ; Laura A. SCHIEVE, Auteur ; Diana SCHENDEL, Auteur ; Lisa A. CROEN, Auteur ; Pankaj CHOPRA, Auteur ; Reid S. ALISCH, Auteur ; Craig J. NEWSCHAFFER, Auteur ; Stephen T. WARREN, Auteur ; Andrew P. FEINBERG, Auteur ; M. Daniele FALLIN, Auteur ; Christine LADD-ACOSTA, Auteur Article en page(s) : 40p. Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/blood/genetics  Case-Control Studies  Child, Preschool  CpG Islands  DNA Methylation  Epigenesis, Genetic  Female  Genome-Wide Association Study  Humans  Male  Autism spectrum disorders  Epigenome  Peripheral blood  Simons Simplex Collection  Study to Explore Early Development Index. décimale : PER Périodiques Résumé : Background: Several reports have suggested a role for epigenetic mechanisms in ASD etiology. Epigenome-wide association studies (EWAS) in autism spectrum disorder (ASD) may shed light on particular biological mechanisms. However, studies of ASD cases versus controls have been limited by post-mortem timing and severely small sample sizes. Reports from in-life sampling of blood or saliva have also been very limited in sample size and/or genomic coverage. We present the largest case-control EWAS for ASD to date, combining data from population-based case-control and case-sibling pair studies. Methods: DNA from 968 blood samples from children in the Study to Explore Early Development (SEED 1) was used to generate epigenome-wide array DNA methylation (DNAm) data at 485,512 CpG sites for 453 cases and 515 controls, using the Illumina 450K Beadchip. The Simons Simplex Collection (SSC) provided 450K array DNAm data on an additional 343 cases and their unaffected siblings. We performed EWAS meta-analysis across results from the two data sets, with adjustment for sex and surrogate variables that reflect major sources of biological variation and technical confounding such as cell type, batch, and ancestry. We compared top EWAS results to those from a previous brain-based analysis. We also tested for enrichment of ASD EWAS CpGs for being targets of meQTL associations using available SNP genotype data in the SEED sample. Findings: In this meta-analysis of blood-based DNA from 796 cases and 858 controls, no single CpG met a Bonferroni discovery threshold of p < 1.12 x 10(- 7). Seven CpGs showed differences at p < 1 x 10(- 5) and 48 at 1 x 10(- 4). Of the top 7, 5 showed brain-based ASD associations as well, often with larger effect sizes, and the top 48 overall showed modest concordance (r = 0.31) in direction of effect with cerebellum samples. Finally, we observed suggestive evidence for enrichment of CpG sites controlled by SNPs (meQTL targets) among the EWAS CpG hits, which was consistent across EWAS and meQTL discovery p value thresholds. Conclusions: No single CpG site showed a large enough DNAm difference between cases and controls to achieve epigenome-wide significance in this sample size. However, our results suggest the potential to observe disease associations from blood-based samples. Among the seven sites achieving suggestive statistical significance, we observed consistent, and stronger, effects at the same sites among brain samples. Discovery-oriented EWAS for ASD using blood samples will likely need even larger samples and unified genetic data to further understand DNAm differences in ASD. En ligne : https://dx.doi.org/10.1186/s13229-018-0224-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371 [article] Case-control meta-analysis of blood DNA methylation and autism spectrum disorder [texte imprimé] / Shan V. ANDREWS, Auteur ; Brooke SHEPPARD, Auteur ; Gayle C. WINDHAM, Auteur ; Laura A. SCHIEVE, Auteur ; Diana SCHENDEL, Auteur ; Lisa A. CROEN, Auteur ; Pankaj CHOPRA, Auteur ; Reid S. ALISCH, Auteur ; Craig J. NEWSCHAFFER, Auteur ; Stephen T. WARREN, Auteur ; Andrew P. FEINBERG, Auteur ; M. Daniele FALLIN, Auteur ; Christine LADD-ACOSTA, Auteur . - 40p. Langues : Anglais (eng) in Molecular Autism > 9 (2018) . - 40p. Mots-clés : Autism Spectrum Disorder/blood/genetics  Case-Control Studies  Child, Preschool  CpG Islands  DNA Methylation  Epigenesis, Genetic  Female  Genome-Wide Association Study  Humans  Male  Autism spectrum disorders  Epigenome  Peripheral blood  Simons Simplex Collection  Study to Explore Early Development Index. décimale : PER Périodiques Résumé : Background: Several reports have suggested a role for epigenetic mechanisms in ASD etiology. Epigenome-wide association studies (EWAS) in autism spectrum disorder (ASD) may shed light on particular biological mechanisms. However, studies of ASD cases versus controls have been limited by post-mortem timing and severely small sample sizes. Reports from in-life sampling of blood or saliva have also been very limited in sample size and/or genomic coverage. We present the largest case-control EWAS for ASD to date, combining data from population-based case-control and case-sibling pair studies. Methods: DNA from 968 blood samples from children in the Study to Explore Early Development (SEED 1) was used to generate epigenome-wide array DNA methylation (DNAm) data at 485,512 CpG sites for 453 cases and 515 controls, using the Illumina 450K Beadchip. The Simons Simplex Collection (SSC) provided 450K array DNAm data on an additional 343 cases and their unaffected siblings. We performed EWAS meta-analysis across results from the two data sets, with adjustment for sex and surrogate variables that reflect major sources of biological variation and technical confounding such as cell type, batch, and ancestry. We compared top EWAS results to those from a previous brain-based analysis. We also tested for enrichment of ASD EWAS CpGs for being targets of meQTL associations using available SNP genotype data in the SEED sample. Findings: In this meta-analysis of blood-based DNA from 796 cases and 858 controls, no single CpG met a Bonferroni discovery threshold of p < 1.12 x 10(- 7). Seven CpGs showed differences at p < 1 x 10(- 5) and 48 at 1 x 10(- 4). Of the top 7, 5 showed brain-based ASD associations as well, often with larger effect sizes, and the top 48 overall showed modest concordance (r = 0.31) in direction of effect with cerebellum samples. Finally, we observed suggestive evidence for enrichment of CpG sites controlled by SNPs (meQTL targets) among the EWAS CpG hits, which was consistent across EWAS and meQTL discovery p value thresholds. Conclusions: No single CpG site showed a large enough DNAm difference between cases and controls to achieve epigenome-wide significance in this sample size. However, our results suggest the potential to observe disease associations from blood-based samples. Among the seven sites achieving suggestive statistical significance, we observed consistent, and stronger, effects at the same sites among brain samples. Discovery-oriented EWAS for ASD using blood samples will likely need even larger samples and unified genetic data to further understand DNAm differences in ASD. En ligne : https://dx.doi.org/10.1186/s13229-018-0224-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371

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