Prenatal exposure to paternal smoking and likelihood for autism spectrum disorder / Bora KIM in Autism, 26-7 (October 2022)  

Public ISBD [article]  inAutism > 26-7 (October 2022) . - p.1946-1959 Titre : Prenatal exposure to paternal smoking and likelihood for autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : Bora KIM, Auteur ; Mina HA, Auteur ; Young Shin KIM, Auteur ; Yun-Joo KOH, Auteur ; Shan DONG, Auteur ; Ho-Jang KWON, Auteur ; Young-Suk KIM, Auteur ; Myung-Ho LIM, Auteur ; Ki-Chung PAIK, Auteur ; Seung-Jin YOO, Auteur ; Hosanna KIM, Auteur ; Patricia S. HONG, Auteur ; Stephan J. SANDERS, Auteur ; Bennett L. LEVENTHAL, Auteur Article en page(s) : p.1946-1959 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/epidemiology/etiology  Causality  Family  Female  Humans  Pregnancy  Prenatal Exposure Delayed Effects/epidemiology/etiology  Risk Factors  Smoking/adverse effects  autism spectrum disorders  environmental factors  risk factor epidemiology  relation to the research presented in this manuscript. Index. décimale : PER Périodiques Résumé : What is Already Known about This Subject: Genetics, (including de novo mutations), environmental factors (including toxic exposures), and their interactions impact autism spectrum disorder etiology. Paternal smoking is a candidate risk for autism spectrum disorder due to biological plausibility, high prevalence, and potential intervention.What This Study Adds: This original study and its replication confirms that paternal factors can substantially contribute to autism spectrum disorder risk for their offspring. It specifically indicates that paternal smoking both before and during pregnancy contributes significantly to autism spectrum disorder risk.Implications for practice, research, or policy: Smoking prevention, especially in pregnancy planning, may decrease autism spectrum disorder risk in offspring. En ligne : http://dx.doi.org/10.1177/13623613211007319 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=484 [article] Prenatal exposure to paternal smoking and likelihood for autism spectrum disorder [Texte imprimé et/ou numérique] / Bora KIM, Auteur ; Mina HA, Auteur ; Young Shin KIM, Auteur ; Yun-Joo KOH, Auteur ; Shan DONG, Auteur ; Ho-Jang KWON, Auteur ; Young-Suk KIM, Auteur ; Myung-Ho LIM, Auteur ; Ki-Chung PAIK, Auteur ; Seung-Jin YOO, Auteur ; Hosanna KIM, Auteur ; Patricia S. HONG, Auteur ; Stephan J. SANDERS, Auteur ; Bennett L. LEVENTHAL, Auteur . - p.1946-1959. Langues : Anglais (eng) in Autism > 26-7 (October 2022) . - p.1946-1959 Mots-clés : Autism Spectrum Disorder/epidemiology/etiology  Causality  Family  Female  Humans  Pregnancy  Prenatal Exposure Delayed Effects/epidemiology/etiology  Risk Factors  Smoking/adverse effects  autism spectrum disorders  environmental factors  risk factor epidemiology  relation to the research presented in this manuscript. Index. décimale : PER Périodiques Résumé : What is Already Known about This Subject: Genetics, (including de novo mutations), environmental factors (including toxic exposures), and their interactions impact autism spectrum disorder etiology. Paternal smoking is a candidate risk for autism spectrum disorder due to biological plausibility, high prevalence, and potential intervention.What This Study Adds: This original study and its replication confirms that paternal factors can substantially contribute to autism spectrum disorder risk for their offspring. It specifically indicates that paternal smoking both before and during pregnancy contributes significantly to autism spectrum disorder risk.Implications for practice, research, or policy: Smoking prevention, especially in pregnancy planning, may decrease autism spectrum disorder risk in offspring. En ligne : http://dx.doi.org/10.1177/13623613211007319 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=484

The female protective effect in autism spectrum disorder is not mediated by a single genetic locus / Jake GOCKLEY in Molecular Autism, (May 2015)  

Public ISBD [article]  inMolecular Autism > (May 2015) . - p.1-10 Titre : The female protective effect in autism spectrum disorder is not mediated by a single genetic locus Type de document : Texte imprimé et/ou numérique Auteurs : Jake GOCKLEY, Auteur ; A. Jeremy WILLSEY, Auteur ; Shan DONG, Auteur ; Joseph D. DOUGHERTY, Auteur ; John N. CONSTANTINO, Auteur ; Stephan J. SANDERS, Auteur Article en page(s) : p.1-10 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : A 4:1 male to female sex bias has consistently been observed in autism spectrum disorder (ASD). Epidemiological and genetic studies suggest a female protective effect (FPE) may account for part of this bias; however, the mechanism of such protection is unknown. Quantitative assessment of ASD symptoms using the Social Responsiveness Scale (SRS) shows a bimodal distribution unique to females in multiplex families. This leads to the hypothesis that a single, common genetic locus on chromosome X might mediate the FPE and produce the ASD sex bias. Such a locus would represent a major therapeutic target and is likely to have been missed by conventional genome-wide association study (GWAS) analysis. En ligne : http://dx.doi.org/10.1186/s13229-015-0014-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277 [article] The female protective effect in autism spectrum disorder is not mediated by a single genetic locus [Texte imprimé et/ou numérique] / Jake GOCKLEY, Auteur ; A. Jeremy WILLSEY, Auteur ; Shan DONG, Auteur ; Joseph D. DOUGHERTY, Auteur ; John N. CONSTANTINO, Auteur ; Stephan J. SANDERS, Auteur . - p.1-10. Langues : Anglais (eng) in Molecular Autism > (May 2015) . - p.1-10 Index. décimale : PER Périodiques Résumé : A 4:1 male to female sex bias has consistently been observed in autism spectrum disorder (ASD). Epidemiological and genetic studies suggest a female protective effect (FPE) may account for part of this bias; however, the mechanism of such protection is unknown. Quantitative assessment of ASD symptoms using the Social Responsiveness Scale (SRS) shows a bimodal distribution unique to females in multiplex families. This leads to the hypothesis that a single, common genetic locus on chromosome X might mediate the FPE and produce the ASD sex bias. Such a locus would represent a major therapeutic target and is likely to have been missed by conventional genome-wide association study (GWAS) analysis. En ligne : http://dx.doi.org/10.1186/s13229-015-0014-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277

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