Meta-analysis-tested formal models of potential mechanisms underlying females’ low autism-spectrum-disorder diagnosis rate compared to males’ / Meng-Ting CHEN in Research in Autism Spectrum Disorders, 98 (October 2022)  

Public ISBD [article]  inResearch in Autism Spectrum Disorders > 98 (October 2022) . - 102047 Titre : Meta-analysis-tested formal models of potential mechanisms underlying females’ low autism-spectrum-disorder diagnosis rate compared to males’ Type de document : Texte imprimé et/ou numérique Auteurs : Meng-Ting CHEN, Auteur ; Xiaopeng LU, Auteur ; Rune J. SIMEONSSON, Auteur ; Marisa E. MARRACCINI, Auteur ; Yen-Ping CHANG, Auteur Article en page(s) : 102047 Langues : Anglais (eng) Mots-clés : Prevalence  Sex difference  Gender  Female  Meta-analysis  Social perception Index. décimale : PER Périodiques Résumé : Background Why is autism spectrum disorder (ASD) less prevalent among females than males? We constructed a statistical model for each of both existing classes of theories, and derived competing predictions for the essentialist expression hypothesis (females express less severe ASD traits so are diagnosed less) against the constructivist perception hypothesis (females’ expressions are socially perceived as less severe so are diagnosed less). Specifically, if the expression hypothesis is true, based on our models, diagnosed females should show less severe symptoms than their male counterparts, whereas the reverse should happen if the perception hypothesis is true. Method We conducted a meta-analysis (Data point N = 117,778 participant N = 16,209) on the differences in ASD symptom severity between females and males diagnosed with ASD, across age groups, IQ ranges, diagnostic criteria, and assessment tools. Results We found strong new evidence that ASD-diagnosed females and males differ little in symptom severity, even in the face of a found publication bias in favor of reporting males’ symptoms relative to females’ and the common understanding of ASD as a so-called male disorder. Conclusions We argue the finding supports both classes of theories, implying that they are similar in size, though different in directions, in creating sex differences in symptom severity for diagnosed individuals. The sex disparity in ASD prevalence likely results from both the biological expression of, and the social perception toward individuals’ ASD symptoms. En ligne : https://doi.org/10.1016/j.rasd.2022.102047 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490 [article] Meta-analysis-tested formal models of potential mechanisms underlying females’ low autism-spectrum-disorder diagnosis rate compared to males’ [Texte imprimé et/ou numérique] / Meng-Ting CHEN, Auteur ; Xiaopeng LU, Auteur ; Rune J. SIMEONSSON, Auteur ; Marisa E. MARRACCINI, Auteur ; Yen-Ping CHANG, Auteur . - 102047. Langues : Anglais (eng) in Research in Autism Spectrum Disorders > 98 (October 2022) . - 102047 Mots-clés : Prevalence  Sex difference  Gender  Female  Meta-analysis  Social perception Index. décimale : PER Périodiques Résumé : Background Why is autism spectrum disorder (ASD) less prevalent among females than males? We constructed a statistical model for each of both existing classes of theories, and derived competing predictions for the essentialist expression hypothesis (females express less severe ASD traits so are diagnosed less) against the constructivist perception hypothesis (females’ expressions are socially perceived as less severe so are diagnosed less). Specifically, if the expression hypothesis is true, based on our models, diagnosed females should show less severe symptoms than their male counterparts, whereas the reverse should happen if the perception hypothesis is true. Method We conducted a meta-analysis (Data point N = 117,778 participant N = 16,209) on the differences in ASD symptom severity between females and males diagnosed with ASD, across age groups, IQ ranges, diagnostic criteria, and assessment tools. Results We found strong new evidence that ASD-diagnosed females and males differ little in symptom severity, even in the face of a found publication bias in favor of reporting males’ symptoms relative to females’ and the common understanding of ASD as a so-called male disorder. Conclusions We argue the finding supports both classes of theories, implying that they are similar in size, though different in directions, in creating sex differences in symptom severity for diagnosed individuals. The sex disparity in ASD prevalence likely results from both the biological expression of, and the social perception toward individuals’ ASD symptoms. En ligne : https://doi.org/10.1016/j.rasd.2022.102047 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490

Single nucleotide polymorphism heritability and differential patterns of genetic overlap between inattention and four neurocognitive factors in youth / Lauren MICALIZZI in Development and Psychopathology, 33-1 (February 2021)  

Public ISBD [article]  inDevelopment and Psychopathology > 33-1 (February 2021) . - p.76-86 Titre : Single nucleotide polymorphism heritability and differential patterns of genetic overlap between inattention and four neurocognitive factors in youth Type de document : Texte imprimé et/ou numérique Auteurs : Lauren MICALIZZI, Auteur ; Leslie A. BRICK, Auteur ; Marisa E. MARRACCINI, Auteur ; Chelsie E. BENCA-BACHMAN, Auteur ; Rohan H. C. PALMER, Auteur ; Valerie S. KNOPIK, Auteur Article en page(s) : p.76-86 Langues : Anglais (eng) Mots-clés : Gcta  adolescence  genetics  heritability  inattention  neurocognitive functioning Index. décimale : PER Périodiques Résumé : Theoretical models of attention-deficit/hyperactivity disorder implicate neurocognitive dysfunction, yet neurocognitive functioning covers a range of abilities that may not all be linked with inattention. This study (a) investigated the single nucleotide polymorphism (SNP) heritability (h2SNP) of inattention and aspects of neurocognitive efficiency (memory, social cognition, executive function, and complex cognition) based on additive genome-wide effects; (b) examined if there were shared genetic effects among inattention and each aspect of neurocognitive efficiency; and (c) conducted an exploratory genome-wide association study to identify genetic regions associated with inattention. The sample included 3,563 participants of the Philadelphia Neurodevelopmental Cohort, a general population sample aged 8-21 years who completed the Penn Neurocognitive Battery. Data on inattention was obtained with the Kiddie Schedule of Affective Disorders (adapted). Genomic relatedness matrix restricted maximum likelihood was implemented in genome-wide complex trait analysis. Analyses revealed significant h2SNP for inattention (20%, SE = 0.08), social cognition (13%, SE = 0.08), memory (17%, SE = 0.08), executive function (25%, SE = 0.08), and complex cognition (24%, SE = 0.08). There was a positive genetic correlation (0.67, SE = 0.37) and a negative residual covariance (-0.23, SE = 0.06) between inattention and social cognition. No SNPs reached genome-wide significance for inattention. Results suggest specificity in genetic overlap among inattention and different aspects of neurocognitive efficiency. En ligne : http://dx.doi.org/10.1017/s0954579419001573 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=442 [article] Single nucleotide polymorphism heritability and differential patterns of genetic overlap between inattention and four neurocognitive factors in youth [Texte imprimé et/ou numérique] / Lauren MICALIZZI, Auteur ; Leslie A. BRICK, Auteur ; Marisa E. MARRACCINI, Auteur ; Chelsie E. BENCA-BACHMAN, Auteur ; Rohan H. C. PALMER, Auteur ; Valerie S. KNOPIK, Auteur . - p.76-86. Langues : Anglais (eng) in Development and Psychopathology > 33-1 (February 2021) . - p.76-86 Mots-clés : Gcta  adolescence  genetics  heritability  inattention  neurocognitive functioning Index. décimale : PER Périodiques Résumé : Theoretical models of attention-deficit/hyperactivity disorder implicate neurocognitive dysfunction, yet neurocognitive functioning covers a range of abilities that may not all be linked with inattention. This study (a) investigated the single nucleotide polymorphism (SNP) heritability (h2SNP) of inattention and aspects of neurocognitive efficiency (memory, social cognition, executive function, and complex cognition) based on additive genome-wide effects; (b) examined if there were shared genetic effects among inattention and each aspect of neurocognitive efficiency; and (c) conducted an exploratory genome-wide association study to identify genetic regions associated with inattention. The sample included 3,563 participants of the Philadelphia Neurodevelopmental Cohort, a general population sample aged 8-21 years who completed the Penn Neurocognitive Battery. Data on inattention was obtained with the Kiddie Schedule of Affective Disorders (adapted). Genomic relatedness matrix restricted maximum likelihood was implemented in genome-wide complex trait analysis. Analyses revealed significant h2SNP for inattention (20%, SE = 0.08), social cognition (13%, SE = 0.08), memory (17%, SE = 0.08), executive function (25%, SE = 0.08), and complex cognition (24%, SE = 0.08). There was a positive genetic correlation (0.67, SE = 0.37) and a negative residual covariance (-0.23, SE = 0.06) between inattention and social cognition. No SNPs reached genome-wide significance for inattention. Results suggest specificity in genetic overlap among inattention and different aspects of neurocognitive efficiency. En ligne : http://dx.doi.org/10.1017/s0954579419001573 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=442

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