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Auteur Daniel J. TANCREDI |
Documents disponibles écrits par cet auteur (5)
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Autism-specific maternal anti-fetal brain autoantibodies are associated with metabolic conditions / Paula KRAKOWIAK in Autism Research, 10-1 (January 2017)
[article]
Titre : Autism-specific maternal anti-fetal brain autoantibodies are associated with metabolic conditions Type de document : Texte imprimé et/ou numérique Auteurs : Paula KRAKOWIAK, Auteur ; Cheryl K. WALKER, Auteur ; Daniel J. TANCREDI, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Judy VAN DE WATER, Auteur Article en page(s) : p.89-98 Langues : Anglais (eng) Mots-clés : autism pregnancy maternal autoantibodies anti-fetal brain autoantibodies metabolic conditions diabetes Index. décimale : PER Périodiques Résumé : Approximately 23% of mothers of children with autism spectrum disorder (ASD) produce specific patterns of autoantibodies to fetal brain proteins that have been detected in only 1% of mothers of typically developing children. The biological mechanisms underlying the development of ASD-specific maternal autoantibodies are poorly understood. We sought to determine whether ASD-specific maternal autoantibodies identified postnatally were associated with metabolic conditions (MCs) during gestation. Participants were 227 mothers of 2–5 year old children with confirmed ASD, enrolled in CHARGE (Childhood Autism Risk from Genetics and the Environment) between January 2003 and April 2008, and from whom blood samples were collected and analyzed for anti-fetal brain autoantibodies (Ab+). MCs included diabetes, hypertensive disorders, and prepregnancy obesity or overweight, ascertained from medical records or structured telephone interviews. Log-linear regression models were performed to estimate prevalence ratios and 95% confidence intervals (CI) based on robust standard errors. Fifty-six (25%) mothers were Ab+. Ab+ prevalence was higher among mothers with diabetes, hypertensive disorders, or overweight compared to healthy mothers, but differences were not statistically significant. In a subset of 145 mothers whose children exhibited severe ASD (31 Ab+), those diagnosed with type 2 or gestational diabetes were 2.7-fold more likely to be Ab+ (95% CI 1.1, 6.6), controlling for delivery payer and smoking. Gestational diabetes specifically was associated with a 3.2-fold increased Ab+ prevalence (95% CI 1.2, 8.6). In this exploratory study, mothers whose children had severe ASD and who experienced diabetes were more likely to have anti-fetal brain autoantibodies 2–5 years later. En ligne : http://dx.doi.org/10.1002/aur.1657 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=303
in Autism Research > 10-1 (January 2017) . - p.89-98[article] Autism-specific maternal anti-fetal brain autoantibodies are associated with metabolic conditions [Texte imprimé et/ou numérique] / Paula KRAKOWIAK, Auteur ; Cheryl K. WALKER, Auteur ; Daniel J. TANCREDI, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Judy VAN DE WATER, Auteur . - p.89-98.
Langues : Anglais (eng)
in Autism Research > 10-1 (January 2017) . - p.89-98
Mots-clés : autism pregnancy maternal autoantibodies anti-fetal brain autoantibodies metabolic conditions diabetes Index. décimale : PER Périodiques Résumé : Approximately 23% of mothers of children with autism spectrum disorder (ASD) produce specific patterns of autoantibodies to fetal brain proteins that have been detected in only 1% of mothers of typically developing children. The biological mechanisms underlying the development of ASD-specific maternal autoantibodies are poorly understood. We sought to determine whether ASD-specific maternal autoantibodies identified postnatally were associated with metabolic conditions (MCs) during gestation. Participants were 227 mothers of 2–5 year old children with confirmed ASD, enrolled in CHARGE (Childhood Autism Risk from Genetics and the Environment) between January 2003 and April 2008, and from whom blood samples were collected and analyzed for anti-fetal brain autoantibodies (Ab+). MCs included diabetes, hypertensive disorders, and prepregnancy obesity or overweight, ascertained from medical records or structured telephone interviews. Log-linear regression models were performed to estimate prevalence ratios and 95% confidence intervals (CI) based on robust standard errors. Fifty-six (25%) mothers were Ab+. Ab+ prevalence was higher among mothers with diabetes, hypertensive disorders, or overweight compared to healthy mothers, but differences were not statistically significant. In a subset of 145 mothers whose children exhibited severe ASD (31 Ab+), those diagnosed with type 2 or gestational diabetes were 2.7-fold more likely to be Ab+ (95% CI 1.1, 6.6), controlling for delivery payer and smoking. Gestational diabetes specifically was associated with a 3.2-fold increased Ab+ prevalence (95% CI 1.2, 8.6). In this exploratory study, mothers whose children had severe ASD and who experienced diabetes were more likely to have anti-fetal brain autoantibodies 2–5 years later. En ligne : http://dx.doi.org/10.1002/aur.1657 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=303 Erratum : Independent and dependent contributions of advanced maternal and paternal ages to autism risk / Janie F. SHELTON in Autism Research, 3-2 (April 2010)
[article]
Titre : Erratum : Independent and dependent contributions of advanced maternal and paternal ages to autism risk Type de document : Texte imprimé et/ou numérique Auteurs : Janie F. SHELTON, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Daniel J. TANCREDI, Auteur Année de publication : 2010 Article en page(s) : p.98 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.135 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=102
in Autism Research > 3-2 (April 2010) . - p.98[article] Erratum : Independent and dependent contributions of advanced maternal and paternal ages to autism risk [Texte imprimé et/ou numérique] / Janie F. SHELTON, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Daniel J. TANCREDI, Auteur . - 2010 . - p.98.
Langues : Anglais (eng)
in Autism Research > 3-2 (April 2010) . - p.98
Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.135 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=102 Independent and dependent contributions of advanced maternal and paternal ages to autism risk / Janie F. SHELTON in Autism Research, 3-1 (February 2010)
[article]
Titre : Independent and dependent contributions of advanced maternal and paternal ages to autism risk Type de document : Texte imprimé et/ou numérique Auteurs : Janie F. SHELTON, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Daniel J. TANCREDI, Auteur Année de publication : 2010 Article en page(s) : p.30-39 Langues : Anglais (eng) Mots-clés : autism maternal-age paternal-age effect-measure-modification attributable-risk advanced-maternal-age advanced-paternal-age interaction Index. décimale : PER Périodiques Résumé : Reports on autism and parental age have yielded conflicting results on whether mothers, fathers, or both, contribute to increased risk. We analyzed restricted strata of parental age in a 10-year California birth cohort to determine the independent or dependent effect from each parent. Autism cases from California Department of Developmental Services records were linked to State birth files (1990-1999). Only singleton births with complete data on parental age and education were included (n=4,947,935, cases=12,159). In multivariate logistic regression models, advancing maternal age increased risk for autism monotonically regardless of the paternal age. Compared with mothers 25-29 years of age, the adjusted odds ratio (aOR) for mothers 40+ years was 1.51 (95% CI: 1.35-1.70), or compared with mothers <25 years of age, aOR=1.77 (95% CI, 1.56-2.00). In contrast, autism risk was associated with advancing paternal age primarily among mothers <30: aOR=1.59 (95% CI, 1.37-1.85) comparing fathers 40+ vs. 25-29 years of age. However, among mothers >30, the aOR was 1.13 (95% CI, 1.01-1.27) for fathers 40+ vs. 25-29 years of age, almost identical to the aOR for fathers <25 years. Based on the first examination of heterogeneity in parental age effects, it appears that women's risk for delivering a child who develops autism increases throughout their reproductive years whereas father's age confers increased risk for autism when mothers are <30, but has little effect when mothers are past age 30. We also calculated that the recent trend towards delayed childbearing contributed approximately a 4.6% increase in autism diagnoses in California over the decade. En ligne : http://dx.doi.org/10.1002/aur.116 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=993
in Autism Research > 3-1 (February 2010) . - p.30-39[article] Independent and dependent contributions of advanced maternal and paternal ages to autism risk [Texte imprimé et/ou numérique] / Janie F. SHELTON, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Daniel J. TANCREDI, Auteur . - 2010 . - p.30-39.
Langues : Anglais (eng)
in Autism Research > 3-1 (February 2010) . - p.30-39
Mots-clés : autism maternal-age paternal-age effect-measure-modification attributable-risk advanced-maternal-age advanced-paternal-age interaction Index. décimale : PER Périodiques Résumé : Reports on autism and parental age have yielded conflicting results on whether mothers, fathers, or both, contribute to increased risk. We analyzed restricted strata of parental age in a 10-year California birth cohort to determine the independent or dependent effect from each parent. Autism cases from California Department of Developmental Services records were linked to State birth files (1990-1999). Only singleton births with complete data on parental age and education were included (n=4,947,935, cases=12,159). In multivariate logistic regression models, advancing maternal age increased risk for autism monotonically regardless of the paternal age. Compared with mothers 25-29 years of age, the adjusted odds ratio (aOR) for mothers 40+ years was 1.51 (95% CI: 1.35-1.70), or compared with mothers <25 years of age, aOR=1.77 (95% CI, 1.56-2.00). In contrast, autism risk was associated with advancing paternal age primarily among mothers <30: aOR=1.59 (95% CI, 1.37-1.85) comparing fathers 40+ vs. 25-29 years of age. However, among mothers >30, the aOR was 1.13 (95% CI, 1.01-1.27) for fathers 40+ vs. 25-29 years of age, almost identical to the aOR for fathers <25 years. Based on the first examination of heterogeneity in parental age effects, it appears that women's risk for delivering a child who develops autism increases throughout their reproductive years whereas father's age confers increased risk for autism when mothers are <30, but has little effect when mothers are past age 30. We also calculated that the recent trend towards delayed childbearing contributed approximately a 4.6% increase in autism diagnoses in California over the decade. En ligne : http://dx.doi.org/10.1002/aur.116 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=993 Joint effects of prenatal air pollutant exposure and maternal folic acid supplementation on risk of autism spectrum disorder / J. GOODRICH AMANDA in Autism Research, 11-1 (January 2018)
[article]
Titre : Joint effects of prenatal air pollutant exposure and maternal folic acid supplementation on risk of autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : J. GOODRICH AMANDA, Auteur ; Heather E. VOLK, Auteur ; Daniel J. TANCREDI, Auteur ; Rob MCCONNELL, Auteur ; W. LURMANN FRED, Auteur ; L. HANSEN ROBIN, Auteur ; Rebecca J. SCHMIDT, Auteur Article en page(s) : p.69-80 Langues : Anglais (eng) Mots-clés : autism ASD folic acid air pollution prenatal exposure environmental exposure Index. décimale : PER Périodiques Résumé : Independent studies report that periconceptional folic acid (FA) may decrease the risk of autism spectrum disorder (ASD) while exposure to air pollution may increase ASD risk. We examined the joint effects of gestational FA and air pollution exposures in association with ASD. We studied 346 ASD cases and 260 typically developing controls from the CHARGE case?control study. Self?reported FA intake for each month of pregnancy was quantified. Estimates of exposure to near roadway air pollution (NRP) and criteria air pollutant measures were assigned based on maternal residential history. Among mothers with high FA intake (>800 ?g) in the first pregnancy month, exposure to increasing levels of all air pollutants, except ozone, during the first trimester was associated with decreased ASD risk, while increased ASD risk was observed for the same pollutant among mothers with low FA intake (?800 ?g). This difference was statistically significant for NO2 (e.g., NO2 and low FA intake: OR=1.53 (0.91, 2.56) vs NO2 and high FA intake: OR=0.74 (0.46, 1.19), P?interaction=0.04). Mothers exposed to higher levels (? median) of any air pollutant during the first trimester of pregnancy and who reported low FA intake were at a higher ASD risk compared to mothers exposed to lower levels of that air pollutant and who reported high first month FA intake. Joint effects showed significant (alpha?0.10) departures from expected interaction for NRP and NO2. Our results suggest that periconceptional FA intake may reduce ASD risk in those with high prenatal air pollution exposure. Further study is needed to replicate these findings in larger sample sizes and to understand mechanisms of this potential relationship.. Autism Res 2018, 11: 69?80. ? 2017 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary We examined interactions between periconceptional folic acid (FA) and air pollution exposure on risk of ASD. Mothers exposed to higher levels of air pollution during the first trimester of pregnancy and who reported low supplemental FA intake during the first pregnancy month were at a higher ASD risk compared to mothers exposed to lower levels of air pollution and who reported high first month FA intake. Our results suggest that periconceptional FA intake may reduce ASD risk in those with high prenatal air pollution exposure. En ligne : https://doi.org/10.1002/aur.1885 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=333
in Autism Research > 11-1 (January 2018) . - p.69-80[article] Joint effects of prenatal air pollutant exposure and maternal folic acid supplementation on risk of autism spectrum disorder [Texte imprimé et/ou numérique] / J. GOODRICH AMANDA, Auteur ; Heather E. VOLK, Auteur ; Daniel J. TANCREDI, Auteur ; Rob MCCONNELL, Auteur ; W. LURMANN FRED, Auteur ; L. HANSEN ROBIN, Auteur ; Rebecca J. SCHMIDT, Auteur . - p.69-80.
Langues : Anglais (eng)
in Autism Research > 11-1 (January 2018) . - p.69-80
Mots-clés : autism ASD folic acid air pollution prenatal exposure environmental exposure Index. décimale : PER Périodiques Résumé : Independent studies report that periconceptional folic acid (FA) may decrease the risk of autism spectrum disorder (ASD) while exposure to air pollution may increase ASD risk. We examined the joint effects of gestational FA and air pollution exposures in association with ASD. We studied 346 ASD cases and 260 typically developing controls from the CHARGE case?control study. Self?reported FA intake for each month of pregnancy was quantified. Estimates of exposure to near roadway air pollution (NRP) and criteria air pollutant measures were assigned based on maternal residential history. Among mothers with high FA intake (>800 ?g) in the first pregnancy month, exposure to increasing levels of all air pollutants, except ozone, during the first trimester was associated with decreased ASD risk, while increased ASD risk was observed for the same pollutant among mothers with low FA intake (?800 ?g). This difference was statistically significant for NO2 (e.g., NO2 and low FA intake: OR=1.53 (0.91, 2.56) vs NO2 and high FA intake: OR=0.74 (0.46, 1.19), P?interaction=0.04). Mothers exposed to higher levels (? median) of any air pollutant during the first trimester of pregnancy and who reported low FA intake were at a higher ASD risk compared to mothers exposed to lower levels of that air pollutant and who reported high first month FA intake. Joint effects showed significant (alpha?0.10) departures from expected interaction for NRP and NO2. Our results suggest that periconceptional FA intake may reduce ASD risk in those with high prenatal air pollution exposure. Further study is needed to replicate these findings in larger sample sizes and to understand mechanisms of this potential relationship.. Autism Res 2018, 11: 69?80. ? 2017 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary We examined interactions between periconceptional folic acid (FA) and air pollution exposure on risk of ASD. Mothers exposed to higher levels of air pollution during the first trimester of pregnancy and who reported low supplemental FA intake during the first pregnancy month were at a higher ASD risk compared to mothers exposed to lower levels of air pollution and who reported high first month FA intake. Our results suggest that periconceptional FA intake may reduce ASD risk in those with high prenatal air pollution exposure. En ligne : https://doi.org/10.1002/aur.1885 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=333 Placental methylome analysis from a prospective autism study / D. I. SCHROEDER in Molecular Autism, 7 (2016)
[article]
Titre : Placental methylome analysis from a prospective autism study Type de document : Texte imprimé et/ou numérique Auteurs : D. I. SCHROEDER, Auteur ; Rebecca J. SCHMIDT, Auteur ; F. K. CRARY-DOOLEY, Auteur ; Cheryl K. WALKER, Auteur ; S. OZONOFF, Auteur ; Daniel J. TANCREDI, Auteur ; I. HERTZ-PICCIOTTO, Auteur ; J. M. LASALLE, Auteur Article en page(s) : 51p. Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/diagnosis/genetics Biomarkers/metabolism Child, Preschool DNA Methylation Early Diagnosis Enhancer Elements, Genetic Epigenesis, Genetic Female Genome, Human Genome-Wide Association Study High-Throughput Nucleotide Sequencing Humans Infant, Newborn Intercellular Signaling Peptides and Proteins/genetics/metabolism Male Membrane Proteins/genetics/metabolism Placenta/metabolism Pregnancy Biomarkers DNA methylation Epigenetics Genomics Methylome Placenta Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASD) are increasingly prevalent neurodevelopmental disorders that are behaviorally diagnosed in early childhood. Most ASD cases likely arise from a complex mixture of genetic and environmental factors, an interface where the epigenetic marks of DNA methylation may be useful as risk biomarkers. The placenta is a potentially useful surrogate tissue characterized by a methylation pattern of partially methylated domains (PMDs) and highly methylated domains (HMDs) reflective of methylation patterns observed in the early embryo. METHODS: In this study, we investigated human term placentas from the MARBLES (Markers of Autism Risk in Babies: Learning Early Signs) prospective study by whole genome bisulfite sequencing. We also examined the utility of PMD/HMDs in detecting methylation differences consistent with ASD diagnosis at age three. RESULTS: We found that while human placental methylomes have highly reproducible PMD and HMD locations, there is a greater variation between individuals in methylation levels over PMDs than HMDs due to both sampling and individual variability. In a comparison of methylation differences in placental samples from 24 ASD and 23 typically developing (TD) children, a HMD containing a putative fetal brain enhancer near DLL1 was found to reach genome-wide significance and was validated for significantly higher methylation in ASD by pyrosequencing. CONCLUSIONS: These results suggest that the placenta could be an informative surrogate tissue for predictive ASD biomarkers in high-risk families. En ligne : http://dx.doi.org/10.1186/s13229-016-0114-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=329
in Molecular Autism > 7 (2016) . - 51p.[article] Placental methylome analysis from a prospective autism study [Texte imprimé et/ou numérique] / D. I. SCHROEDER, Auteur ; Rebecca J. SCHMIDT, Auteur ; F. K. CRARY-DOOLEY, Auteur ; Cheryl K. WALKER, Auteur ; S. OZONOFF, Auteur ; Daniel J. TANCREDI, Auteur ; I. HERTZ-PICCIOTTO, Auteur ; J. M. LASALLE, Auteur . - 51p.
Langues : Anglais (eng)
in Molecular Autism > 7 (2016) . - 51p.
Mots-clés : Autism Spectrum Disorder/diagnosis/genetics Biomarkers/metabolism Child, Preschool DNA Methylation Early Diagnosis Enhancer Elements, Genetic Epigenesis, Genetic Female Genome, Human Genome-Wide Association Study High-Throughput Nucleotide Sequencing Humans Infant, Newborn Intercellular Signaling Peptides and Proteins/genetics/metabolism Male Membrane Proteins/genetics/metabolism Placenta/metabolism Pregnancy Biomarkers DNA methylation Epigenetics Genomics Methylome Placenta Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASD) are increasingly prevalent neurodevelopmental disorders that are behaviorally diagnosed in early childhood. Most ASD cases likely arise from a complex mixture of genetic and environmental factors, an interface where the epigenetic marks of DNA methylation may be useful as risk biomarkers. The placenta is a potentially useful surrogate tissue characterized by a methylation pattern of partially methylated domains (PMDs) and highly methylated domains (HMDs) reflective of methylation patterns observed in the early embryo. METHODS: In this study, we investigated human term placentas from the MARBLES (Markers of Autism Risk in Babies: Learning Early Signs) prospective study by whole genome bisulfite sequencing. We also examined the utility of PMD/HMDs in detecting methylation differences consistent with ASD diagnosis at age three. RESULTS: We found that while human placental methylomes have highly reproducible PMD and HMD locations, there is a greater variation between individuals in methylation levels over PMDs than HMDs due to both sampling and individual variability. In a comparison of methylation differences in placental samples from 24 ASD and 23 typically developing (TD) children, a HMD containing a putative fetal brain enhancer near DLL1 was found to reach genome-wide significance and was validated for significantly higher methylation in ASD by pyrosequencing. CONCLUSIONS: These results suggest that the placenta could be an informative surrogate tissue for predictive ASD biomarkers in high-risk families. En ligne : http://dx.doi.org/10.1186/s13229-016-0114-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=329