Comparing autism phenotypes in children born extremely preterm and born at term / Robert M. JOSEPH in Autism Research, 16-3 (March 2023)  

Public ISBD [article]  inAutism Research > 16-3 (March 2023) . - p.653-666 Titre : Comparing autism phenotypes in children born extremely preterm and born at term Type de document : Texte imprimé et/ou numérique Auteurs : Robert M. JOSEPH, Auteur ; Emily R. LAI, Auteur ; Somer BISHOP, Auteur ; Joe YI, Auteur ; Margaret L. BAUMAN, Auteur ; Jean A. FRAZIER, Auteur ; Hudson P. SANTOS JR, Auteur ; Laurie M. DOUGLAS, Auteur ; Karl K. C. KUBAN, Auteur ; Rebecca C. FRY, Auteur ; T. Michael O'SHEA, Auteur Article en page(s) : p.653-666 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Abstract Children born preterm are at increased risk for autism spectrum disorder (ASD). There is limited knowledge about whether ASD phenotypes in children born preterm differ from children born at term. The objective of this study was to compare ASD core symptoms and associated characteristics among extremely preterm (EP) and term-born children with ASD. EP participants (n = 59) from the Extremely Low Gestational Age Newborn Study who met diagnostic criteria for ASD at approximately 10?years of age were matched with term-born participants from the Simons Simplex Collection on age, sex, spoken language level, and nonverbal IQ. Core ASD symptomatology was evaluated with the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS). Developmental milestones, anthropometrics, seizure disorder, and psychiatric symptoms were also investigated. The EP group had lower parent-reported symptom scores on ADI-R verbal communication, specifically stereotyped language, and restricted, repetitive behaviors. There were no between-group differences on ADI-R nonverbal communication and ADI-R reciprocal social interaction or with direct observation on the ADOS-2. The EP group was more likely to have delayed speech milestones and lower physical growth parameters. Results from female-only analyses were similar to those from whole-group analyses. In sum, behavioral presentation was similar between EP and IQ- and sex-matched term-born children assessed at age 10?years, with the exception of less severe retrospectively reported stereotyped behaviors, lower physical growth parameters, and increased delays in language milestones among EP-born children with ASD. En ligne : https://doi.org/10.1002/aur.2885 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=499 [article] Comparing autism phenotypes in children born extremely preterm and born at term [Texte imprimé et/ou numérique] / Robert M. JOSEPH, Auteur ; Emily R. LAI, Auteur ; Somer BISHOP, Auteur ; Joe YI, Auteur ; Margaret L. BAUMAN, Auteur ; Jean A. FRAZIER, Auteur ; Hudson P. SANTOS JR, Auteur ; Laurie M. DOUGLAS, Auteur ; Karl K. C. KUBAN, Auteur ; Rebecca C. FRY, Auteur ; T. Michael O'SHEA, Auteur . - p.653-666. Langues : Anglais (eng) in Autism Research > 16-3 (March 2023) . - p.653-666 Index. décimale : PER Périodiques Résumé : Abstract Children born preterm are at increased risk for autism spectrum disorder (ASD). There is limited knowledge about whether ASD phenotypes in children born preterm differ from children born at term. The objective of this study was to compare ASD core symptoms and associated characteristics among extremely preterm (EP) and term-born children with ASD. EP participants (n = 59) from the Extremely Low Gestational Age Newborn Study who met diagnostic criteria for ASD at approximately 10?years of age were matched with term-born participants from the Simons Simplex Collection on age, sex, spoken language level, and nonverbal IQ. Core ASD symptomatology was evaluated with the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS). Developmental milestones, anthropometrics, seizure disorder, and psychiatric symptoms were also investigated. The EP group had lower parent-reported symptom scores on ADI-R verbal communication, specifically stereotyped language, and restricted, repetitive behaviors. There were no between-group differences on ADI-R nonverbal communication and ADI-R reciprocal social interaction or with direct observation on the ADOS-2. The EP group was more likely to have delayed speech milestones and lower physical growth parameters. Results from female-only analyses were similar to those from whole-group analyses. In sum, behavioral presentation was similar between EP and IQ- and sex-matched term-born children assessed at age 10?years, with the exception of less severe retrospectively reported stereotyped behaviors, lower physical growth parameters, and increased delays in language milestones among EP-born children with ASD. En ligne : https://doi.org/10.1002/aur.2885 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=499

Evidence for the placenta-brain axis: multi-omic kernel aggregation predicts intellectual and social impairment in children born extremely preterm / Hudson P. Jr SANTOS in Molecular Autism, 11 (2020)  

Public ISBD [article]  inMolecular Autism > 11 (2020) Titre : Evidence for the placenta-brain axis: multi-omic kernel aggregation predicts intellectual and social impairment in children born extremely preterm Type de document : Texte imprimé et/ou numérique Auteurs : Hudson P. Jr SANTOS, Auteur ; Arjun BHATTACHARYA, Auteur ; Robert M. JOSEPH, Auteur ; Lisa SMEESTER, Auteur ; Karl C. K. KUBAN, Auteur ; Carmen J. MARSIT, Auteur ; T. Michael O'SHEA, Auteur ; Rebecca C. FRY, Auteur Langues : Anglais (eng) Mots-clés : Differential expression analysis  Epigenome-wide association  Multi-omic aggregation  Placental gene regulation  Prenatal neurodevelopmental programming  Social and cognitive impairment Index. décimale : PER Périodiques Résumé : BACKGROUND: Children born extremely preterm are at heightened risk for intellectual and social impairment, including Autism Spectrum Disorder (ASD). There is increasing evidence for a key role of the placenta in prenatal developmental programming, suggesting that the placenta may, in part, contribute to origins of neurodevelopmental outcomes. METHODS: We examined associations between placental transcriptomic and epigenomic profiles and assessed their ability to predict intellectual and social impairment at age 10 years in 379 children from the Extremely Low Gestational Age Newborn (ELGAN) cohort. Assessment of intellectual ability (IQ) and social function was completed with the Differential Ability Scales-II and Social Responsiveness Scale (SRS), respectively. Examining IQ and SRS allows for studying ASD risk beyond the diagnostic criteria, as IQ and SRS are continuous measures strongly correlated with ASD. Genome-wide mRNA, CpG methylation and miRNA were assayeds with the Illumina Hiseq 2500, HTG EdgeSeq miRNA Whole Transcriptome Assay, and Illumina EPIC/850 K array, respectively. We conducted genome-wide differential analyses of placental mRNA, miRNA, and CpG methylation data. These molecular features were then integrated for a predictive analysis of IQ and SRS outcomes using kernel aggregation regression. We lastly examined associations between ASD and the multi-omic-predicted component of IQ and SRS. RESULTS: Genes with important roles in neurodevelopment and placental tissue organization were associated with intellectual and social impairment. Kernel aggregations of placental multi-omics strongly predicted intellectual and social function, explaining approximately 8% and 12% of variance in SRS and IQ scores via cross-validation, respectively. Predicted in-sample SRS and IQ showed significant positive and negative associations with ASD case-control status. LIMITATIONS: The ELGAN cohort comprises children born pre-term, and generalization may be affected by unmeasured confounders associated with low gestational age. We conducted external validation of predictive models, though the sample size (N = 49) and the scope of the available out-sample placental dataset are limited. Further validation of the models is merited. CONCLUSIONS: Aggregating information from biomarkers within and among molecular data types improves prediction of complex traits like social and intellectual ability in children born extremely preterm, suggesting that traits within the placenta-brain axis may be omnigenic. En ligne : http://dx.doi.org/10.1186/s13229-020-00402-w Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438 [article] Evidence for the placenta-brain axis: multi-omic kernel aggregation predicts intellectual and social impairment in children born extremely preterm [Texte imprimé et/ou numérique] / Hudson P. Jr SANTOS, Auteur ; Arjun BHATTACHARYA, Auteur ; Robert M. JOSEPH, Auteur ; Lisa SMEESTER, Auteur ; Karl C. K. KUBAN, Auteur ; Carmen J. MARSIT, Auteur ; T. Michael O'SHEA, Auteur ; Rebecca C. FRY, Auteur. Langues : Anglais (eng) in Molecular Autism > 11 (2020) Mots-clés : Differential expression analysis  Epigenome-wide association  Multi-omic aggregation  Placental gene regulation  Prenatal neurodevelopmental programming  Social and cognitive impairment Index. décimale : PER Périodiques Résumé : BACKGROUND: Children born extremely preterm are at heightened risk for intellectual and social impairment, including Autism Spectrum Disorder (ASD). There is increasing evidence for a key role of the placenta in prenatal developmental programming, suggesting that the placenta may, in part, contribute to origins of neurodevelopmental outcomes. METHODS: We examined associations between placental transcriptomic and epigenomic profiles and assessed their ability to predict intellectual and social impairment at age 10 years in 379 children from the Extremely Low Gestational Age Newborn (ELGAN) cohort. Assessment of intellectual ability (IQ) and social function was completed with the Differential Ability Scales-II and Social Responsiveness Scale (SRS), respectively. Examining IQ and SRS allows for studying ASD risk beyond the diagnostic criteria, as IQ and SRS are continuous measures strongly correlated with ASD. Genome-wide mRNA, CpG methylation and miRNA were assayeds with the Illumina Hiseq 2500, HTG EdgeSeq miRNA Whole Transcriptome Assay, and Illumina EPIC/850 K array, respectively. We conducted genome-wide differential analyses of placental mRNA, miRNA, and CpG methylation data. These molecular features were then integrated for a predictive analysis of IQ and SRS outcomes using kernel aggregation regression. We lastly examined associations between ASD and the multi-omic-predicted component of IQ and SRS. RESULTS: Genes with important roles in neurodevelopment and placental tissue organization were associated with intellectual and social impairment. Kernel aggregations of placental multi-omics strongly predicted intellectual and social function, explaining approximately 8% and 12% of variance in SRS and IQ scores via cross-validation, respectively. Predicted in-sample SRS and IQ showed significant positive and negative associations with ASD case-control status. LIMITATIONS: The ELGAN cohort comprises children born pre-term, and generalization may be affected by unmeasured confounders associated with low gestational age. We conducted external validation of predictive models, though the sample size (N = 49) and the scope of the available out-sample placental dataset are limited. Further validation of the models is merited. CONCLUSIONS: Aggregating information from biomarkers within and among molecular data types improves prediction of complex traits like social and intellectual ability in children born extremely preterm, suggesting that traits within the placenta-brain axis may be omnigenic. En ligne : http://dx.doi.org/10.1186/s13229-020-00402-w Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438

Maternal tobacco smoking and offspring autism spectrum disorder or traits in ECHO cohorts / Irva HERTZ-PICCIOTTO in Autism Research, 15-3 (March 2022)  

Public ISBD [article]  inAutism Research > 15-3 (March 2022) . - p.551-569 Titre : Maternal tobacco smoking and offspring autism spectrum disorder or traits in ECHO cohorts Type de document : Texte imprimé et/ou numérique Auteurs : Irva HERTZ-PICCIOTTO, Auteur ; Susan A. KORRICK, Auteur ; Christine LADD-ACOSTA, Auteur ; Margaret R. KARAGAS, Auteur ; Kristen LYALL, Auteur ; Rebecca J. SCHMIDT, Auteur ; Anne L. DUNLOP, Auteur ; Lisa A. CROEN, Auteur ; Dana DABELEA, Auteur ; Julie L. DANIELS, Auteur ; Cristiane S. DUARTE, Auteur ; M. Daniele FALLIN, Auteur ; Catherine J. KARR, Auteur ; Barry LESTER, Auteur ; Leslie D. LEVE, Auteur ; Yijun LI, Auteur ; Monica MCGRATH, Auteur ; Xuejuan NING, Auteur ; Emily OKEN, Auteur ; Sharon K. SAGIV, Auteur ; Sheela SATHYANARAYA, Auteur ; Frances TYLAVSKY, Auteur ; Heather E. VOLK, Auteur ; Lauren S. WAKSCHLAG, Auteur ; Mingyu ZHANG, Auteur ; T. Michael O'SHEA, Auteur ; Rashelle J. MUSCI, Auteur ; program collaborators for Environmental influences on Child Health OUTCOMES, Auteur Article en page(s) : p.551-569 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Abstract Given inconsistent evidence on preconception or prenatal tobacco use and offspring autism spectrum disorder (ASD), this study assessed associations of maternal smoking with ASD and ASD-related traits. Among 72 cohorts in the Environmental Influences on Child Health Outcomes consortium, 11 had ASD diagnosis and prenatal tobaccosmoking (n = 8648). and 7 had Social Responsiveness Scale (SRS) scores of ASD traits (n = 2399). Cohorts had diagnoses alone (6), traits alone (2), or both (5). Diagnoses drew from parent/caregiver report, review of records, or standardized instruments. Regression models estimated smoking-related odds ratios (ORs) for diagnoses and standardized mean differences for SRS scores. Cohort-specific ORs were meta-analyzed. Overall, maternal smoking was unassociated with child ASD (adjusted OR, 1.08; 95% confidence interval [CI], 0.72?1.61). However, heterogeneity across studies was strong: preterm cohorts showed reduced ASD risk for exposed children. After excluding preterm cohorts (biased by restrictions on causal intermediate and exposure opportunity) and small cohorts (very few ASD cases in either smoking category), the adjusted OR for ASD from maternal smoking was 1.44 (95% CI, 1.02?2.03). Children of smoking (versus non-smoking) mothers had more ASD traits (SRS T-score?+?2.37 points, 95% CI, 0.73?4.01 points), with results homogeneous across cohorts. Maternal preconception/prenatal smoking was consistently associated with quantitative ASD traits and modestly associated with ASD diagnosis among sufficiently powered United States cohorts of non-preterm children. Limitations resulting from self-reported smoking and unmeasured confounders preclude definitive conclusions. Nevertheless, counseling on potential and known risks to the child from maternal smoking is warranted for pregnant women and pregnancy planners. Lay Summary Evidence on the association between maternal prenatal smoking and the child's risk for autism spectrum disorder has been conflicting, with some studies reporting harmful effects, and others finding reduced risks. Our analysis of children in the ECHO consortium found that maternal prenatal tobacco smoking is consistently associated with an increase in autism-related symptoms in the general population and modestly associated with elevated risk for a diagnosis of autism spectrum disorder when looking at a combined analysis from multiple studies that each included both pre- and full-term births. However, this study is not proof of a causal connection. Future studies to clarify the role of smoking in autism-like behaviors or autism diagnoses should collect more reliable data on smoking and measure other exposures or lifestyle factors that might have confounded our results. En ligne : https://doi.org/10.1002/aur.2665 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473 [article] Maternal tobacco smoking and offspring autism spectrum disorder or traits in ECHO cohorts [Texte imprimé et/ou numérique] / Irva HERTZ-PICCIOTTO, Auteur ; Susan A. KORRICK, Auteur ; Christine LADD-ACOSTA, Auteur ; Margaret R. KARAGAS, Auteur ; Kristen LYALL, Auteur ; Rebecca J. SCHMIDT, Auteur ; Anne L. DUNLOP, Auteur ; Lisa A. CROEN, Auteur ; Dana DABELEA, Auteur ; Julie L. DANIELS, Auteur ; Cristiane S. DUARTE, Auteur ; M. Daniele FALLIN, Auteur ; Catherine J. KARR, Auteur ; Barry LESTER, Auteur ; Leslie D. LEVE, Auteur ; Yijun LI, Auteur ; Monica MCGRATH, Auteur ; Xuejuan NING, Auteur ; Emily OKEN, Auteur ; Sharon K. SAGIV, Auteur ; Sheela SATHYANARAYA, Auteur ; Frances TYLAVSKY, Auteur ; Heather E. VOLK, Auteur ; Lauren S. WAKSCHLAG, Auteur ; Mingyu ZHANG, Auteur ; T. Michael O'SHEA, Auteur ; Rashelle J. MUSCI, Auteur ; program collaborators for Environmental influences on Child Health OUTCOMES, Auteur . - p.551-569. Langues : Anglais (eng) in Autism Research > 15-3 (March 2022) . - p.551-569 Index. décimale : PER Périodiques Résumé : Abstract Given inconsistent evidence on preconception or prenatal tobacco use and offspring autism spectrum disorder (ASD), this study assessed associations of maternal smoking with ASD and ASD-related traits. Among 72 cohorts in the Environmental Influences on Child Health Outcomes consortium, 11 had ASD diagnosis and prenatal tobaccosmoking (n = 8648). and 7 had Social Responsiveness Scale (SRS) scores of ASD traits (n = 2399). Cohorts had diagnoses alone (6), traits alone (2), or both (5). Diagnoses drew from parent/caregiver report, review of records, or standardized instruments. Regression models estimated smoking-related odds ratios (ORs) for diagnoses and standardized mean differences for SRS scores. Cohort-specific ORs were meta-analyzed. Overall, maternal smoking was unassociated with child ASD (adjusted OR, 1.08; 95% confidence interval [CI], 0.72?1.61). However, heterogeneity across studies was strong: preterm cohorts showed reduced ASD risk for exposed children. After excluding preterm cohorts (biased by restrictions on causal intermediate and exposure opportunity) and small cohorts (very few ASD cases in either smoking category), the adjusted OR for ASD from maternal smoking was 1.44 (95% CI, 1.02?2.03). Children of smoking (versus non-smoking) mothers had more ASD traits (SRS T-score?+?2.37 points, 95% CI, 0.73?4.01 points), with results homogeneous across cohorts. Maternal preconception/prenatal smoking was consistently associated with quantitative ASD traits and modestly associated with ASD diagnosis among sufficiently powered United States cohorts of non-preterm children. Limitations resulting from self-reported smoking and unmeasured confounders preclude definitive conclusions. Nevertheless, counseling on potential and known risks to the child from maternal smoking is warranted for pregnant women and pregnancy planners. Lay Summary Evidence on the association between maternal prenatal smoking and the child's risk for autism spectrum disorder has been conflicting, with some studies reporting harmful effects, and others finding reduced risks. Our analysis of children in the ECHO consortium found that maternal prenatal tobacco smoking is consistently associated with an increase in autism-related symptoms in the general population and modestly associated with elevated risk for a diagnosis of autism spectrum disorder when looking at a combined analysis from multiple studies that each included both pre- and full-term births. However, this study is not proof of a causal connection. Future studies to clarify the role of smoking in autism-like behaviors or autism diagnoses should collect more reliable data on smoking and measure other exposures or lifestyle factors that might have confounded our results. En ligne : https://doi.org/10.1002/aur.2665 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473

A multi-omic approach identifies an autism spectrum disorder (ASD) regulatory complex of functional epimutations in placentas from children born preterm / Anastasia N. FREEDMAN in Autism Research, 16-5 (May 2023)  

Public ISBD [article]  inAutism Research > 16-5 (May 2023) . - p.918-934 Titre : A multi-omic approach identifies an autism spectrum disorder (ASD) regulatory complex of functional epimutations in placentas from children born preterm Type de document : Texte imprimé et/ou numérique Auteurs : Anastasia N. FREEDMAN, Auteur ; Jeliyah CLARK, Auteur ; Lauren A. EAVES, Auteur ; Kyle ROELL, Auteur ; Ali ORAN, Auteur ; Lauren KOVAL, Auteur ; Julia RAGER, Auteur ; Hudson P. SANTOS JR., Auteur ; Karl KUBAN, Auteur ; Robert M. JOSEPH, Auteur ; Jean FRAZIER, Auteur ; Carmen J. MARSIT, Auteur ; Amber A. BURT, Auteur ; T. Michael O'SHEA, Auteur ; Rebecca C. FRY, Auteur Article en page(s) : p.918-934 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Abstract Children born preterm are at heightened risk of neurodevelopmental impairments, including Autism Spectrum Disorder (ASD). The placenta is a key regulator of neurodevelopmental processes, though the precise underlying molecular mechanisms remain unclear. Here, we employed a multi-omic approach to identify placental transcriptomic and epigenetic modifications related to ASD diagnosis at age 10, among children born preterm. Working with the extremely low gestational age (ELGAN) cohort, we hypothesized that a pro-inflammatory placental environment would be predictive of ASD diagnosis at age 10. Placental messenger RNA (mRNA) expression, CpG methylation, and microRNA (miRNA) expression were compared among 368 ELGANs (28 children diagnosed with ASD and 340 children without ASD). A total of 111 genes displayed expression levels in the placenta that were associated with ASD. Within these ASD-associated genes is an ASD regulatory complex comprising key genes that predicted ASD case status. Genes with expression that predicted ASD case status included Ewing Sarcoma Breakpoint Region 1 (EWSR1) (OR: 6.57 (95% CI: 2.34, 23.58)) and Bromodomain Adjacent To Zinc Finger Domain 2A (BAZ2A) (OR: 0.12 (95% CI: 0.03, 0.35)). Moreover, of the 111 ASD-associated genes, nine (8.1%) displayed associations with CpG methylation levels, while 14 (12.6%) displayed associations with miRNA expression levels. Among these, LRR Binding FLII Interacting Protein 1 (LRRFIP1) was identified as being under the control of both CpG methylation and miRNAs, displaying an OR of 0.42 (95% CI: 0.17, 0.95). This gene, as well as others identified as having functional epimutations, plays a critical role in immune system regulation and inflammatory response. In summary, a multi-omic approach was used to identify functional epimutations in the placenta that are associated with the development of ASD in children born preterm, highlighting future avenues for intervention. En ligne : http://dx.doi.org/https://doi.org/10.1002/aur.2915 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=503 [article] A multi-omic approach identifies an autism spectrum disorder (ASD) regulatory complex of functional epimutations in placentas from children born preterm [Texte imprimé et/ou numérique] / Anastasia N. FREEDMAN, Auteur ; Jeliyah CLARK, Auteur ; Lauren A. EAVES, Auteur ; Kyle ROELL, Auteur ; Ali ORAN, Auteur ; Lauren KOVAL, Auteur ; Julia RAGER, Auteur ; Hudson P. SANTOS JR., Auteur ; Karl KUBAN, Auteur ; Robert M. JOSEPH, Auteur ; Jean FRAZIER, Auteur ; Carmen J. MARSIT, Auteur ; Amber A. BURT, Auteur ; T. Michael O'SHEA, Auteur ; Rebecca C. FRY, Auteur . - p.918-934. Langues : Anglais (eng) in Autism Research > 16-5 (May 2023) . - p.918-934 Index. décimale : PER Périodiques Résumé : Abstract Children born preterm are at heightened risk of neurodevelopmental impairments, including Autism Spectrum Disorder (ASD). The placenta is a key regulator of neurodevelopmental processes, though the precise underlying molecular mechanisms remain unclear. Here, we employed a multi-omic approach to identify placental transcriptomic and epigenetic modifications related to ASD diagnosis at age 10, among children born preterm. Working with the extremely low gestational age (ELGAN) cohort, we hypothesized that a pro-inflammatory placental environment would be predictive of ASD diagnosis at age 10. Placental messenger RNA (mRNA) expression, CpG methylation, and microRNA (miRNA) expression were compared among 368 ELGANs (28 children diagnosed with ASD and 340 children without ASD). A total of 111 genes displayed expression levels in the placenta that were associated with ASD. Within these ASD-associated genes is an ASD regulatory complex comprising key genes that predicted ASD case status. Genes with expression that predicted ASD case status included Ewing Sarcoma Breakpoint Region 1 (EWSR1) (OR: 6.57 (95% CI: 2.34, 23.58)) and Bromodomain Adjacent To Zinc Finger Domain 2A (BAZ2A) (OR: 0.12 (95% CI: 0.03, 0.35)). Moreover, of the 111 ASD-associated genes, nine (8.1%) displayed associations with CpG methylation levels, while 14 (12.6%) displayed associations with miRNA expression levels. Among these, LRR Binding FLII Interacting Protein 1 (LRRFIP1) was identified as being under the control of both CpG methylation and miRNAs, displaying an OR of 0.42 (95% CI: 0.17, 0.95). This gene, as well as others identified as having functional epimutations, plays a critical role in immune system regulation and inflammatory response. In summary, a multi-omic approach was used to identify functional epimutations in the placenta that are associated with the development of ASD in children born preterm, highlighting future avenues for intervention. En ligne : http://dx.doi.org/https://doi.org/10.1002/aur.2915 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=503

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