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

Cord and Early Childhood Plasma Adiponectin Levels and Autism Risk: A Prospective Birth Cohort Study / R. RAGHAVAN in Journal of Autism and Developmental Disorders, 49-1 (January 2019)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 49-1 (January 2019) . - p.173-184 Titre : Cord and Early Childhood Plasma Adiponectin Levels and Autism Risk: A Prospective Birth Cohort Study Type de document : Texte imprimé et/ou numérique Auteurs : R. RAGHAVAN, Auteur ; M. D. FALLIN, Auteur ; X. HONG, Auteur ; G. WANG, Auteur ; Y. JI, Auteur ; E. A. STUART, Auteur ; D. PAIGE, Auteur ; X. WANG, Auteur Article en page(s) : p.173-184 Langues : Anglais (eng) Mots-clés : Adiponectin  Autism  Cytokines  Preterm birth Index. décimale : PER Périodiques Résumé : Emerging research suggests that adiponectin, a cytokine produced by adipose tissue, may be implicated in ASD. In this prospective birth cohort study (n = 847), we assessed the association between cord, early childhood plasma adiponectin and the risk of developing ASD. ASD was defined based on ICD codes of physician diagnosis. Cord adiponectin levels were inversely associated with ASD risk (aOR 0.50; 95% CI 0.33, 0.77), independent of preterm birth, early childhood adiponectin and other known ASD risk factors. Early childhood adiponectin, assessed prior to ASD diagnosis, was associated with lower risk of ASD, which attenuated after adjusting for cord adiponectin, indicating the relative importance of cord adiponectin in ASD risk. Further research is warranted to confirm our findings and elucidate biological mechanisms. En ligne : http://dx.doi.org/10.1007/s10803-018-3688-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=376 [article] Cord and Early Childhood Plasma Adiponectin Levels and Autism Risk: A Prospective Birth Cohort Study [Texte imprimé et/ou numérique] / R. RAGHAVAN, Auteur ; M. D. FALLIN, Auteur ; X. HONG, Auteur ; G. WANG, Auteur ; Y. JI, Auteur ; E. A. STUART, Auteur ; D. PAIGE, Auteur ; X. WANG, Auteur . - p.173-184. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 49-1 (January 2019) . - p.173-184 Mots-clés : Adiponectin  Autism  Cytokines  Preterm birth Index. décimale : PER Périodiques Résumé : Emerging research suggests that adiponectin, a cytokine produced by adipose tissue, may be implicated in ASD. In this prospective birth cohort study (n = 847), we assessed the association between cord, early childhood plasma adiponectin and the risk of developing ASD. ASD was defined based on ICD codes of physician diagnosis. Cord adiponectin levels were inversely associated with ASD risk (aOR 0.50; 95% CI 0.33, 0.77), independent of preterm birth, early childhood adiponectin and other known ASD risk factors. Early childhood adiponectin, assessed prior to ASD diagnosis, was associated with lower risk of ASD, which attenuated after adjusting for cord adiponectin, indicating the relative importance of cord adiponectin in ASD risk. Further research is warranted to confirm our findings and elucidate biological mechanisms. En ligne : http://dx.doi.org/10.1007/s10803-018-3688-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=376

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

Fetal and Infancy Growth Pattern, Cord and Early Childhood Plasma Leptin, and Development of Autism Spectrum Disorder in the Boston Birth Cohort / R. RAGHAVAN in Autism Research, 11-10 (October 2018)  

Public ISBD [article]  inAutism Research > 11-10 (October 2018) . - p.1416-1431 Titre : Fetal and Infancy Growth Pattern, Cord and Early Childhood Plasma Leptin, and Development of Autism Spectrum Disorder in the Boston Birth Cohort Type de document : Texte imprimé et/ou numérique Auteurs : R. RAGHAVAN, Auteur ; Barry S. ZUCKERMAN, Auteur ; X. HONG, Auteur ; G. WANG, Auteur ; Y. JI, Auteur ; D. PAIGE, Auteur ; J. DIBARI, Auteur ; C. ZHANG, Auteur ; M. D. FALLIN, Auteur ; X. WANG, Auteur Article en page(s) : p.1416-1431 Langues : Anglais (eng) Mots-clés : autism  birth weight for gestational age  leptin  rapid weight gain in infancy Index. décimale : PER Périodiques Résumé : Leptin is a proinflammatory cytokine that plays an important role in energy homeostasis. Emerging evidence suggests that leptin levels are altered in children with autism spectrum disorder (ASD); however, this has not been studied prospectively. Rapid growth during infancy and early childhood has been implicated in ASD, but the evidence is inconsistent. As leptin is involved in growth and is a potential risk factor for ASD, we explored the associations between (a) cord, early childhood leptin and ASD; and (b) birth weight for gestational age, early childhood weight gain, and ASD. We also assessed the mediating role of leptin in the relationship between weight gain during infancy and ASD. This study was conducted in a sample of 822 subjects from the Boston Birth Cohort. ASD was defined from diagnostic codes in electronic medical records. Extremely rapid weight gain during infancy was associated with a greater ASD risk and this persisted after adjusting for potential confounders (aOR: 3.11; 95% CI: 1.37, 7.07). Similarly, children that had higher plasma leptin levels, prior to ASD diagnosis, had an increased ASD risk in both unadjusted and adjusted models (aOR: 7.87; 95% CI: 2.06, 30.04). Further, early childhood leptin indirectly mediated the relationship between rapid weight gain and ASD. No associations were found between birth weight for gestational age, cord leptin and risk of ASD. Our findings provide a basis to further explore whether the combination of early life growth pattern and a biomarker such as leptin can predict ASD earlier. Autism Res 2018, 11: 1416-1431. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Is early life growth and a biomarker leptin related to ASD risk? To answer this question, we followed 822 children from birth and found that those who gained weight very quickly in infancy, had higher leptin levels in early childhood, had a greater chance of later ASD diagnosis. More research is needed to see if infant's weight gain pattern along with a biomarker (such as leptin) can be used to identify children with ASD sooner. En ligne : http://dx.doi.org/10.1002/aur.2011 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=369 [article] Fetal and Infancy Growth Pattern, Cord and Early Childhood Plasma Leptin, and Development of Autism Spectrum Disorder in the Boston Birth Cohort [Texte imprimé et/ou numérique] / R. RAGHAVAN, Auteur ; Barry S. ZUCKERMAN, Auteur ; X. HONG, Auteur ; G. WANG, Auteur ; Y. JI, Auteur ; D. PAIGE, Auteur ; J. DIBARI, Auteur ; C. ZHANG, Auteur ; M. D. FALLIN, Auteur ; X. WANG, Auteur . - p.1416-1431. Langues : Anglais (eng) in Autism Research > 11-10 (October 2018) . - p.1416-1431 Mots-clés : autism  birth weight for gestational age  leptin  rapid weight gain in infancy Index. décimale : PER Périodiques Résumé : Leptin is a proinflammatory cytokine that plays an important role in energy homeostasis. Emerging evidence suggests that leptin levels are altered in children with autism spectrum disorder (ASD); however, this has not been studied prospectively. Rapid growth during infancy and early childhood has been implicated in ASD, but the evidence is inconsistent. As leptin is involved in growth and is a potential risk factor for ASD, we explored the associations between (a) cord, early childhood leptin and ASD; and (b) birth weight for gestational age, early childhood weight gain, and ASD. We also assessed the mediating role of leptin in the relationship between weight gain during infancy and ASD. This study was conducted in a sample of 822 subjects from the Boston Birth Cohort. ASD was defined from diagnostic codes in electronic medical records. Extremely rapid weight gain during infancy was associated with a greater ASD risk and this persisted after adjusting for potential confounders (aOR: 3.11; 95% CI: 1.37, 7.07). Similarly, children that had higher plasma leptin levels, prior to ASD diagnosis, had an increased ASD risk in both unadjusted and adjusted models (aOR: 7.87; 95% CI: 2.06, 30.04). Further, early childhood leptin indirectly mediated the relationship between rapid weight gain and ASD. No associations were found between birth weight for gestational age, cord leptin and risk of ASD. Our findings provide a basis to further explore whether the combination of early life growth pattern and a biomarker such as leptin can predict ASD earlier. Autism Res 2018, 11: 1416-1431. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Is early life growth and a biomarker leptin related to ASD risk? To answer this question, we followed 822 children from birth and found that those who gained weight very quickly in infancy, had higher leptin levels in early childhood, had a greater chance of later ASD diagnosis. More research is needed to see if infant's weight gain pattern along with a biomarker (such as leptin) can be used to identify children with ASD sooner. En ligne : http://dx.doi.org/10.1002/aur.2011 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=369

Gastrointestinal Symptoms in 2- to 5-Year-Old Children in the Study to Explore Early Development / A. M. REYNOLDS in Journal of Autism and Developmental Disorders, 51-11 (November 2021)  

Permalink

Glutathione pathway gene variation and risk of autism spectrum disorders / K. BOWERS in Journal of Neurodevelopmental Disorders, 3-2 (June 2011)  

Permalink

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

Permalink

Maternal diabetes and hypertensive disorders in association with autism spectrum disorder / C. CORDERO in Autism Research, 12-6 (June 2019)  

Permalink

A meta-analysis of two high-risk prospective cohort studies reveals autism-specific transcriptional changes to chromatin, autoimmune, and environmental response genes in umbilical cord blood / C. E. MORDAUNT in Molecular Autism, 10 (2019)  

Permalink

Umbilical cord blood androgen levels and ASD-related phenotypes at 12 and 36 months in an enriched risk cohort study / B. Y. PARK in Molecular Autism, 8 (2017)  

Permalink

---

1 (1 - 11 / 11)