Association between atopic diseases and neurodevelopmental disabilities in a longitudinal birth cohort / Xueqi QU in Autism Research, 15-4 (April 2022)  

Public ISBD [article]  inAutism Research > 15-4 (April 2022) . - p.740-750 Titre : Association between atopic diseases and neurodevelopmental disabilities in a longitudinal birth cohort Type de document : Texte imprimé et/ou numérique Auteurs : Xueqi QU, Auteur ; Li-Ching LEE, Auteur ; Christine LADD-ACOSTA, Auteur ; Xiumei HONG, Auteur ; Yuelong JI, Auteur ; Luther G. KALB, Auteur ; Heather E. VOLK, Auteur ; Xiaobin WANG, Auteur Article en page(s) : p.740-750 Langues : Anglais (eng) Mots-clés : Asthma/complications/epidemiology  Attention Deficit Disorder with Hyperactivity/complications/epidemiology  Autism Spectrum Disorder/complications/epidemiology  Birth Cohort  Child  Dermatitis, Atopic/complications/epidemiology  Female  Humans  Infant, Newborn  Risk Factors  atopic diseases  children  neurodevelopmental disability  the United States  relevant to this article to disclose. Index. décimale : PER Périodiques Résumé : Reports on the association between the prevalence of atopic diseases and neurodevelopmental disabilities (NDs) have been inconsistent in the literature. We investigated whether autism spectrum disorder (ASD), attention deficit-hyperactivity disorders (ADHD), and other NDs are more prevalent in children with asthma, atopic dermatitis (AD) and allergic rhinitis (AR) compared to those without specific atopic conditions. A total of 2580 children enrolled at birth were followed prospectively, of which 119 have ASD, 423 have ADHD, 765 have other NDs, and 1273 have no NDs. Atopic diseases and NDs were defined based on physician diagnoses in electronic medical records. Logistic regressions adjusting for maternal and child characteristics estimated the associations between NDs (i.e., ASD, ADHD, and other NDs) and asthma, AD and AR, respectively. Children with asthma, AD or AR had a greater likelihood of having ADHD or other NDs compared with children without specific atopic conditions. The association between ASD and asthma diminished after adjusting for maternal and child factors. Either mothers or children having atopic conditions and both mothers and children with atopic conditions were associated with a higher prevalence of ADHD in children, compared with neither mothers nor children having atopic conditions. Children diagnosed with multiple atopic diseases were more likely to have NDs compared with those without or with only one type of atopic disease. In conclusion, in this U.S. urban birth cohort, children with atopic diseases had a higher co-morbidity of NDs. The findings have implications for etiologic research that searches for common early life antecedents of NDs and atopic conditions. Findings from this study also should raise awareness among health care providers and parents about the possible co-occurrence of both NDs and atopic conditions, which calls for coordinated efforts to screen, prevent and manage NDs and atopic conditions. En ligne : https://dx.doi.org/10.1002/aur.2680 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473 [article] Association between atopic diseases and neurodevelopmental disabilities in a longitudinal birth cohort [Texte imprimé et/ou numérique] / Xueqi QU, Auteur ; Li-Ching LEE, Auteur ; Christine LADD-ACOSTA, Auteur ; Xiumei HONG, Auteur ; Yuelong JI, Auteur ; Luther G. KALB, Auteur ; Heather E. VOLK, Auteur ; Xiaobin WANG, Auteur . - p.740-750. Langues : Anglais (eng) in Autism Research > 15-4 (April 2022) . - p.740-750 Mots-clés : Asthma/complications/epidemiology  Attention Deficit Disorder with Hyperactivity/complications/epidemiology  Autism Spectrum Disorder/complications/epidemiology  Birth Cohort  Child  Dermatitis, Atopic/complications/epidemiology  Female  Humans  Infant, Newborn  Risk Factors  atopic diseases  children  neurodevelopmental disability  the United States  relevant to this article to disclose. Index. décimale : PER Périodiques Résumé : Reports on the association between the prevalence of atopic diseases and neurodevelopmental disabilities (NDs) have been inconsistent in the literature. We investigated whether autism spectrum disorder (ASD), attention deficit-hyperactivity disorders (ADHD), and other NDs are more prevalent in children with asthma, atopic dermatitis (AD) and allergic rhinitis (AR) compared to those without specific atopic conditions. A total of 2580 children enrolled at birth were followed prospectively, of which 119 have ASD, 423 have ADHD, 765 have other NDs, and 1273 have no NDs. Atopic diseases and NDs were defined based on physician diagnoses in electronic medical records. Logistic regressions adjusting for maternal and child characteristics estimated the associations between NDs (i.e., ASD, ADHD, and other NDs) and asthma, AD and AR, respectively. Children with asthma, AD or AR had a greater likelihood of having ADHD or other NDs compared with children without specific atopic conditions. The association between ASD and asthma diminished after adjusting for maternal and child factors. Either mothers or children having atopic conditions and both mothers and children with atopic conditions were associated with a higher prevalence of ADHD in children, compared with neither mothers nor children having atopic conditions. Children diagnosed with multiple atopic diseases were more likely to have NDs compared with those without or with only one type of atopic disease. In conclusion, in this U.S. urban birth cohort, children with atopic diseases had a higher co-morbidity of NDs. The findings have implications for etiologic research that searches for common early life antecedents of NDs and atopic conditions. Findings from this study also should raise awareness among health care providers and parents about the possible co-occurrence of both NDs and atopic conditions, which calls for coordinated efforts to screen, prevent and manage NDs and atopic conditions. En ligne : https://dx.doi.org/10.1002/aur.2680 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473

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

Public ISBD [article]  inAutism Research > 15-12 (December 2022) . - p.2359-2370 Titre : Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children Type de document : Texte imprimé et/ou numérique Auteurs : Ashley Y. SONG, Auteur ; Kelly BAKULSKI, Auteur ; Jason I. FEINBERG, Auteur ; Craig NEWSCHAFFER, Auteur ; Lisa A. CROEN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Homayoon FARZADEGAN, Auteur ; Kristen LYALL, Auteur ; M Daniele FALLIN, Auteur ; Heather E. VOLK, Auteur ; Christine LADD-ACOSTA, Auteur Article en page(s) : p.2359-2370 Langues : Anglais (eng) Mots-clés : Child  Male  Pregnancy  Female  Humans  Autism Spectrum Disorder/epidemiology/genetics  Prospective Studies  Parents  Cognition  Biological Products  Epigenesis, Genetic  DNA methylation  age acceleration  autism spectrum disorder  autism-related traits  biologic age  epigenetic age  parental age Index. décimale : PER Périodiques Résumé : Parental age is a known risk factor for autism spectrum disorder (ASD), however, studies to identify the biologic changes underpinning this association are limited. In recent years, "epigenetic clock" algorithms have been developed to estimate biologic age and to evaluate how the epigenetic aging impacts health and disease. In this study, we examined the relationship between parental epigenetic aging and their child's prospective risk of ASD and autism related quantitative traits in the Early Autism Risk Longitudinal Investigation study. Estimates of epigenetic age were computed using three robust clock algorithms and DNA methylation measures from the Infinium HumanMethylation450k platform for maternal blood and paternal blood specimens collected during pregnancy. Epigenetic age acceleration was defined as the residual of regressing chronological age on epigenetic age while accounting for cell type proportions. Multinomial logistic regression and linear regression models were completed adjusting for potential confounders for both maternal epigenetic age acceleration (n = 163) and paternal epigenetic age acceleration (n = 80). We found accelerated epigenetic aging in mothers estimated by Hannum's clock was significantly associated with lower cognitive ability and function in offspring at 12 months, as measured by Mullen Scales of Early Learning scores (Î2 = -1.66, 95% CI: -3.28, -0.04 for a one-unit increase). We also observed a marginal association between accelerated maternal epigenetic aging by Horvath's clock and increased odds of ASD in offspring at 36 months of age (aOR = 1.12, 95% CI: 0.99, 1.26). By contrast, fathers accelerated aging was marginally associated with decreased ASD risk in their offspring (aOR = 0.83, 95% CI: 0.68, 1.01). Our findings suggest epigenetic aging could play a role in parental age risks on child brain development. En ligne : http://dx.doi.org/10.1002/aur.2822 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=488 [article] Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children [Texte imprimé et/ou numérique] / Ashley Y. SONG, Auteur ; Kelly BAKULSKI, Auteur ; Jason I. FEINBERG, Auteur ; Craig NEWSCHAFFER, Auteur ; Lisa A. CROEN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Homayoon FARZADEGAN, Auteur ; Kristen LYALL, Auteur ; M Daniele FALLIN, Auteur ; Heather E. VOLK, Auteur ; Christine LADD-ACOSTA, Auteur . - p.2359-2370. Langues : Anglais (eng) in Autism Research > 15-12 (December 2022) . - p.2359-2370 Mots-clés : Child  Male  Pregnancy  Female  Humans  Autism Spectrum Disorder/epidemiology/genetics  Prospective Studies  Parents  Cognition  Biological Products  Epigenesis, Genetic  DNA methylation  age acceleration  autism spectrum disorder  autism-related traits  biologic age  epigenetic age  parental age Index. décimale : PER Périodiques Résumé : Parental age is a known risk factor for autism spectrum disorder (ASD), however, studies to identify the biologic changes underpinning this association are limited. In recent years, "epigenetic clock" algorithms have been developed to estimate biologic age and to evaluate how the epigenetic aging impacts health and disease. In this study, we examined the relationship between parental epigenetic aging and their child's prospective risk of ASD and autism related quantitative traits in the Early Autism Risk Longitudinal Investigation study. Estimates of epigenetic age were computed using three robust clock algorithms and DNA methylation measures from the Infinium HumanMethylation450k platform for maternal blood and paternal blood specimens collected during pregnancy. Epigenetic age acceleration was defined as the residual of regressing chronological age on epigenetic age while accounting for cell type proportions. Multinomial logistic regression and linear regression models were completed adjusting for potential confounders for both maternal epigenetic age acceleration (n = 163) and paternal epigenetic age acceleration (n = 80). We found accelerated epigenetic aging in mothers estimated by Hannum's clock was significantly associated with lower cognitive ability and function in offspring at 12 months, as measured by Mullen Scales of Early Learning scores (Î2 = -1.66, 95% CI: -3.28, -0.04 for a one-unit increase). We also observed a marginal association between accelerated maternal epigenetic aging by Horvath's clock and increased odds of ASD in offspring at 36 months of age (aOR = 1.12, 95% CI: 0.99, 1.26). By contrast, fathers accelerated aging was marginally associated with decreased ASD risk in their offspring (aOR = 0.83, 95% CI: 0.68, 1.01). Our findings suggest epigenetic aging could play a role in parental age risks on child brain development. En ligne : http://dx.doi.org/10.1002/aur.2822 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=488

Case-control meta-analysis of blood DNA methylation and autism spectrum disorder / S. 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 et/ou numérique Auteurs : S. V. ANDREWS, Auteur ; B. SHEPPARD, Auteur ; G. C. WINDHAM, Auteur ; Laura A. SCHIEVE, Auteur ; Diana SCHENDEL, Auteur ; Lisa A. CROEN, Auteur ; P. CHOPRA, Auteur ; R. S. ALISCH, Auteur ; C. J. NEWSCHAFFER, Auteur ; S. T. WARREN, Auteur ; A. P. FEINBERG, Auteur ; M. D. 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 et/ou numérique] / S. V. ANDREWS, Auteur ; B. SHEPPARD, Auteur ; G. C. WINDHAM, Auteur ; Laura A. SCHIEVE, Auteur ; Diana SCHENDEL, Auteur ; Lisa A. CROEN, Auteur ; P. CHOPRA, Auteur ; R. S. ALISCH, Auteur ; C. J. NEWSCHAFFER, Auteur ; S. T. WARREN, Auteur ; A. P. FEINBERG, Auteur ; M. D. 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

Distributional Properties and Criterion Validity of a Shortened Version of the Social Responsiveness Scale: Results from the ECHO Program and Implications for Social Communication Research / K. LYALL in Journal of Autism and Developmental Disorders, 51-7 (July 2021)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 51-7 (July 2021) . - p.2241-2253 Titre : Distributional Properties and Criterion Validity of a Shortened Version of the Social Responsiveness Scale: Results from the ECHO Program and Implications for Social Communication Research Type de document : Texte imprimé et/ou numérique Auteurs : K. LYALL, Auteur ; M. HOSSEINI, Auteur ; Christine LADD-ACOSTA, Auteur ; X. NING, Auteur ; D. CATELLIER, Auteur ; John N. CONSTANTINO, Auteur ; Lisa A. CROEN, Auteur ; A. J. KAAT, Auteur ; Kelly N. BOTTERON, Auteur ; Nicole R. BUSH, Auteur ; Stephen R. DAGER, Auteur ; C. S. DUARTE, Auteur ; M. D. FALLIN, Auteur ; Heather C. HAZLETT, Auteur ; I. HERTZ-PICCIOTTO, Auteur ; R. M. JOSEPH, Auteur ; Margaret R. KARAGAS, Auteur ; S. KORRICK, Auteur ; R. LANDA, Auteur ; D. MESSINGER, Auteur ; E. OKEN, Auteur ; S. OZONOFF, Auteur ; J. PIVEN, Auteur ; J. PANDEY, Auteur ; Sheela SATHYANARAYA, Auteur ; Robert T. SCHULTZ, Auteur ; T. ST JOHN, Auteur ; R. SCHMIDT, Auteur ; Heather E. VOLK, Auteur ; C. J. NEWSCHAFFER, Auteur Article en page(s) : p.2241-2253 Langues : Anglais (eng) Mots-clés : Adolescent  Area Under Curve  Autism Spectrum Disorder/diagnosis  Child  Child, Preschool  Communication  Female  Humans  Male  Psychiatric Status Rating Scales/standards  Psychometrics  Reproducibility of Results  Social Behavior  Autism spectrum disorder  Quantitative traits  Social Responsiveness Scale  Social communication Index. décimale : PER Périodiques Résumé : Prior work proposed a shortened version of the Social Responsiveness Scale (SRS), a commonly used quantitative measure of social communication traits. We used data from 3031 participants (including 190 ASD cases) from the Environmental Influences on Child Health Outcomes (ECHO) Program to compare distributional properties and criterion validity of 16-item "short" to 65-item "full" SRS scores. Results demonstrated highly overlapping distributions of short and full scores. Both scores separated case from non-case individuals by approximately two standard deviations. ASD prediction was nearly identical for short and full scores (area under the curve values of 0.87, 0.86 respectively). Findings support comparability of shortened and full scores, suggesting opportunities to increase efficiency. Future work should confirm additional psychometric properties of short scores. En ligne : http://dx.doi.org/10.1007/s10803-020-04667-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=452 [article] Distributional Properties and Criterion Validity of a Shortened Version of the Social Responsiveness Scale: Results from the ECHO Program and Implications for Social Communication Research [Texte imprimé et/ou numérique] / K. LYALL, Auteur ; M. HOSSEINI, Auteur ; Christine LADD-ACOSTA, Auteur ; X. NING, Auteur ; D. CATELLIER, Auteur ; John N. CONSTANTINO, Auteur ; Lisa A. CROEN, Auteur ; A. J. KAAT, Auteur ; Kelly N. BOTTERON, Auteur ; Nicole R. BUSH, Auteur ; Stephen R. DAGER, Auteur ; C. S. DUARTE, Auteur ; M. D. FALLIN, Auteur ; Heather C. HAZLETT, Auteur ; I. HERTZ-PICCIOTTO, Auteur ; R. M. JOSEPH, Auteur ; Margaret R. KARAGAS, Auteur ; S. KORRICK, Auteur ; R. LANDA, Auteur ; D. MESSINGER, Auteur ; E. OKEN, Auteur ; S. OZONOFF, Auteur ; J. PIVEN, Auteur ; J. PANDEY, Auteur ; Sheela SATHYANARAYA, Auteur ; Robert T. SCHULTZ, Auteur ; T. ST JOHN, Auteur ; R. SCHMIDT, Auteur ; Heather E. VOLK, Auteur ; C. J. NEWSCHAFFER, Auteur . - p.2241-2253. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 51-7 (July 2021) . - p.2241-2253 Mots-clés : Adolescent  Area Under Curve  Autism Spectrum Disorder/diagnosis  Child  Child, Preschool  Communication  Female  Humans  Male  Psychiatric Status Rating Scales/standards  Psychometrics  Reproducibility of Results  Social Behavior  Autism spectrum disorder  Quantitative traits  Social Responsiveness Scale  Social communication Index. décimale : PER Périodiques Résumé : Prior work proposed a shortened version of the Social Responsiveness Scale (SRS), a commonly used quantitative measure of social communication traits. We used data from 3031 participants (including 190 ASD cases) from the Environmental Influences on Child Health Outcomes (ECHO) Program to compare distributional properties and criterion validity of 16-item "short" to 65-item "full" SRS scores. Results demonstrated highly overlapping distributions of short and full scores. Both scores separated case from non-case individuals by approximately two standard deviations. ASD prediction was nearly identical for short and full scores (area under the curve values of 0.87, 0.86 respectively). Findings support comparability of shortened and full scores, suggesting opportunities to increase efficiency. Future work should confirm additional psychometric properties of short scores. En ligne : http://dx.doi.org/10.1007/s10803-020-04667-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=452

Evaluating the interrelations between the autism polygenic score and psychiatric family history in risk for autism / Diana SCHENDEL in Autism Research, 15-1 (January 2022)  

Public ISBD [article]  inAutism Research > 15-1 (January 2022) . - p.171-182 Titre : Evaluating the interrelations between the autism polygenic score and psychiatric family history in risk for autism Type de document : Texte imprimé et/ou numérique Auteurs : Diana SCHENDEL, Auteur ; T. MUNK LAURSEN, Auteur ; C. ALBIÑANA, Auteur ; B. VILHJALMSSON, Auteur ; Christine LADD-ACOSTA, Auteur ; M. D. FALLIN, Auteur ; Kelly S. BENKE, Auteur ; B. LEE, Auteur ; J. GROVE, Auteur ; Amy E. KALKBRENNER, Auteur ; L. EJLSKOV, Auteur ; D. HOUGAARD, Auteur ; Jonas BYBJERG-GRAUHOLM, Auteur ; M. BAEKVAD-HANSEN, Auteur ; A. D. BØRGLUM, Auteur ; T. WERGE, Auteur ; M. NORDENTOFT, Auteur ; P. B. MORTENSEN, Auteur ; E. AGERBO, Auteur Article en page(s) : p.171-182 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/genetics  Autistic Disorder/genetics  Case-Control Studies  Humans  Multifactorial Inheritance/genetics  Risk Factors  Siblings  autism spectrum disorder  case-control studies  family history  genetic risk factors  polygenic risk score Index. décimale : PER Périodiques Résumé : Psychiatric family history or a high autism polygenic risk score (PRS) have been separately linked to autism spectrum disorder (ASD) risk. The study aimed to simultaneously consider psychiatric family history and individual autism genetic liability (PRS) in autism risk. We performed a case-control study of all Denmark singleton births, May 1981-December 2005, in Denmark at their first birthday and a known mother. Cases were diagnosed with ASD before 2013 and controls comprised a random sample of 30,000 births without ASD, excluding persons with non-Denmark-born parents, missing ASD PRS, non-European ancestry. Adjusted odds ratios (aOR) were estimated for ASD by PRS decile and by psychiatric history in parents or full siblings (8 mutually-exclusive categories) using logistic regression. Adjusted ASD PRS z-score least-squares means were estimated by psychiatric family history category. ASD risk (11,339 ASD cases; 20,175 controls) from ASD PRS was not substantially altered after accounting for psychiatric family history (e.g., ASD PRS 10th decile aOR: 2.35 (95% CI 2.11-2.63) before vs 2.11 (95% CI 1.91-2.40) after adjustment) nor from psychiatric family history after accounting for ASD PRS (e.g., ASD family history aOR: 6.73 (95% CI 5.89-7.68) before vs 6.32 (95% CI 5.53-7.22) after adjustment). ASD risk from ASD PRS varied slightly by psychiatric family history. While ASD risk from psychiatric family history was not accounted for by ASD PRS and vice versa, risk overlap between the two factors will likely increase as measures of genetic risk improve. The two factors are best viewed as complementary measures of family-based autism risk. LAY SUMMARY: Autism risk from a history of mental disorders in the immediate family was not explained by a measure of individual genetic risk (autism polygenic risk score) and vice versa. That is, genetic risk did not appear to overlap family history risk. As genetic measures for autism improve then the overlap in autism risk from family history versus genetic factors will likely increase, but further study may be needed to fully determine the components of risk and how they are inter-related between these key family factors. Meanwhile, the two factors may be best viewed as complementary measures of autism family-based risk. En ligne : http://dx.doi.org/10.1002/aur.2629 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450 [article] Evaluating the interrelations between the autism polygenic score and psychiatric family history in risk for autism [Texte imprimé et/ou numérique] / Diana SCHENDEL, Auteur ; T. MUNK LAURSEN, Auteur ; C. ALBIÑANA, Auteur ; B. VILHJALMSSON, Auteur ; Christine LADD-ACOSTA, Auteur ; M. D. FALLIN, Auteur ; Kelly S. BENKE, Auteur ; B. LEE, Auteur ; J. GROVE, Auteur ; Amy E. KALKBRENNER, Auteur ; L. EJLSKOV, Auteur ; D. HOUGAARD, Auteur ; Jonas BYBJERG-GRAUHOLM, Auteur ; M. BAEKVAD-HANSEN, Auteur ; A. D. BØRGLUM, Auteur ; T. WERGE, Auteur ; M. NORDENTOFT, Auteur ; P. B. MORTENSEN, Auteur ; E. AGERBO, Auteur . - p.171-182. Langues : Anglais (eng) in Autism Research > 15-1 (January 2022) . - p.171-182 Mots-clés : Autism Spectrum Disorder/genetics  Autistic Disorder/genetics  Case-Control Studies  Humans  Multifactorial Inheritance/genetics  Risk Factors  Siblings  autism spectrum disorder  case-control studies  family history  genetic risk factors  polygenic risk score Index. décimale : PER Périodiques Résumé : Psychiatric family history or a high autism polygenic risk score (PRS) have been separately linked to autism spectrum disorder (ASD) risk. The study aimed to simultaneously consider psychiatric family history and individual autism genetic liability (PRS) in autism risk. We performed a case-control study of all Denmark singleton births, May 1981-December 2005, in Denmark at their first birthday and a known mother. Cases were diagnosed with ASD before 2013 and controls comprised a random sample of 30,000 births without ASD, excluding persons with non-Denmark-born parents, missing ASD PRS, non-European ancestry. Adjusted odds ratios (aOR) were estimated for ASD by PRS decile and by psychiatric history in parents or full siblings (8 mutually-exclusive categories) using logistic regression. Adjusted ASD PRS z-score least-squares means were estimated by psychiatric family history category. ASD risk (11,339 ASD cases; 20,175 controls) from ASD PRS was not substantially altered after accounting for psychiatric family history (e.g., ASD PRS 10th decile aOR: 2.35 (95% CI 2.11-2.63) before vs 2.11 (95% CI 1.91-2.40) after adjustment) nor from psychiatric family history after accounting for ASD PRS (e.g., ASD family history aOR: 6.73 (95% CI 5.89-7.68) before vs 6.32 (95% CI 5.53-7.22) after adjustment). ASD risk from ASD PRS varied slightly by psychiatric family history. While ASD risk from psychiatric family history was not accounted for by ASD PRS and vice versa, risk overlap between the two factors will likely increase as measures of genetic risk improve. The two factors are best viewed as complementary measures of family-based autism risk. LAY SUMMARY: Autism risk from a history of mental disorders in the immediate family was not explained by a measure of individual genetic risk (autism polygenic risk score) and vice versa. That is, genetic risk did not appear to overlap family history risk. As genetic measures for autism improve then the overlap in autism risk from family history versus genetic factors will likely increase, but further study may be needed to fully determine the components of risk and how they are inter-related between these key family factors. Meanwhile, the two factors may be best viewed as complementary measures of autism family-based risk. En ligne : http://dx.doi.org/10.1002/aur.2629 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450

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