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Autism spectrum disorder polygenic scores are associated with every day executive function in children admitted for clinical assessment / Tonje TORSKE in Autism Research, 13-2 (February 2020)
[article]
Titre : Autism spectrum disorder polygenic scores are associated with every day executive function in children admitted for clinical assessment Type de document : Texte imprimé et/ou numérique Auteurs : Tonje TORSKE, Auteur ; Terje NAERLAND, Auteur ; Francesco BETTELLA, Auteur ; Thomas BJELLA, Auteur ; Eva MALT, Auteur ; Anne Lise HOYLAND, Auteur ; Nina STENBERG, Auteur ; Merete Glenne OIE, Auteur ; Ole A. ANDREASSEN, Auteur Article en page(s) : p.207-220 Langues : Anglais (eng) Mots-clés : attention deficit/hyperactivity disorder autism spectrum disorder behavior rating inventory of executive function executive function polygenic score Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) and other neurodevelopmental disorders (NDs) are behaviorally defined disorders with overlapping clinical features that are often associated with higher-order cognitive dysfunction, particularly executive dysfunction. Our aim was to determine if the polygenic score (PGS) for ASD is associated with parent-reported executive dysfunction in everyday life using the Behavior Rating Inventory of Executive Function (BRIEF). Furthermore, we investigated if PGS for general intelligence (INT) and attention deficit/hyperactivity disorder (ADHD) also correlate with BRIEF. We included 176 children, adolescents and young adults aged 5-22 years with full-scale intelligence quotient (IQ) above 70. All were admitted for clinical assessment of ASD symptoms and 68% obtained an ASD diagnosis. We found a significant difference between low and high ASD PGS groups in the BRIEF behavior regulation index (BRI) (P = 0.015, Cohen's d = 0.69). A linear regression model accounting for age, sex, full-scale IQ, Social Responsiveness Scale (SRS) total score, ASD, ADHD and INT PGS groups as well as genetic principal components, significantly predicted the BRI score; F(11,130) = 8.142, P < 0.001, R(2) = 0.41 (unadjusted). Only SRS total (P < 0.001), ASD PGS 0.1 group (P = 0.018), and sex (P = 0.022) made a significant contribution to the model. This suggests that the common ASD risk gene variants have a stronger association to behavioral regulation aspects of executive dysfunction than ADHD risk or INT variants in a clinical sample with ASD symptoms. Autism Res 2020, 13: 207-220. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: People with autism spectrum disorder (ASD) often have difficulties with higher-order cognitive processes that regulate thoughts and actions during goal-directed behavior, also known as executive function (EF). We studied the association between genetics related to ASD and EF and found a relation between high polygenic score (PGS) for ASD and difficulties with behavior regulation aspects of EF in children and adolescents under assessment for ASD. Furthermore, high PGS for general intelligence was related to social problems. En ligne : http://dx.doi.org/10.1002/aur.2207 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=420
in Autism Research > 13-2 (February 2020) . - p.207-220[article] Autism spectrum disorder polygenic scores are associated with every day executive function in children admitted for clinical assessment [Texte imprimé et/ou numérique] / Tonje TORSKE, Auteur ; Terje NAERLAND, Auteur ; Francesco BETTELLA, Auteur ; Thomas BJELLA, Auteur ; Eva MALT, Auteur ; Anne Lise HOYLAND, Auteur ; Nina STENBERG, Auteur ; Merete Glenne OIE, Auteur ; Ole A. ANDREASSEN, Auteur . - p.207-220.
Langues : Anglais (eng)
in Autism Research > 13-2 (February 2020) . - p.207-220
Mots-clés : attention deficit/hyperactivity disorder autism spectrum disorder behavior rating inventory of executive function executive function polygenic score Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) and other neurodevelopmental disorders (NDs) are behaviorally defined disorders with overlapping clinical features that are often associated with higher-order cognitive dysfunction, particularly executive dysfunction. Our aim was to determine if the polygenic score (PGS) for ASD is associated with parent-reported executive dysfunction in everyday life using the Behavior Rating Inventory of Executive Function (BRIEF). Furthermore, we investigated if PGS for general intelligence (INT) and attention deficit/hyperactivity disorder (ADHD) also correlate with BRIEF. We included 176 children, adolescents and young adults aged 5-22 years with full-scale intelligence quotient (IQ) above 70. All were admitted for clinical assessment of ASD symptoms and 68% obtained an ASD diagnosis. We found a significant difference between low and high ASD PGS groups in the BRIEF behavior regulation index (BRI) (P = 0.015, Cohen's d = 0.69). A linear regression model accounting for age, sex, full-scale IQ, Social Responsiveness Scale (SRS) total score, ASD, ADHD and INT PGS groups as well as genetic principal components, significantly predicted the BRI score; F(11,130) = 8.142, P < 0.001, R(2) = 0.41 (unadjusted). Only SRS total (P < 0.001), ASD PGS 0.1 group (P = 0.018), and sex (P = 0.022) made a significant contribution to the model. This suggests that the common ASD risk gene variants have a stronger association to behavioral regulation aspects of executive dysfunction than ADHD risk or INT variants in a clinical sample with ASD symptoms. Autism Res 2020, 13: 207-220. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: People with autism spectrum disorder (ASD) often have difficulties with higher-order cognitive processes that regulate thoughts and actions during goal-directed behavior, also known as executive function (EF). We studied the association between genetics related to ASD and EF and found a relation between high polygenic score (PGS) for ASD and difficulties with behavior regulation aspects of EF in children and adolescents under assessment for ASD. Furthermore, high PGS for general intelligence was related to social problems. En ligne : http://dx.doi.org/10.1002/aur.2207 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=420 Neurodevelopmental and genetic determinants of exposure to adversity among youth at risk for mental illness / Alyson ZWICKER in Journal of Child Psychology and Psychiatry, 61-5 (May 2020)
[article]
Titre : Neurodevelopmental and genetic determinants of exposure to adversity among youth at risk for mental illness Type de document : Texte imprimé et/ou numérique Auteurs : Alyson ZWICKER, Auteur ; Lynn E. MACKENZIE, Auteur ; Vladislav DROBININ, Auteur ; Amina M. BAGHER, Auteur ; Emily HOWES VALLIS, Auteur ; Lukas PROPPER, Auteur ; Alexa BAGNELL, Auteur ; Sabina ABIDI, Auteur ; Barbara PAVLOVA, Auteur ; Martin ALDA, Auteur ; Eileen M. DENOVAN-WRIGHT, Auteur ; Rudolf UHER, Auteur Article en page(s) : p.536-544 Langues : Anglais (eng) Mots-clés : Attention-deficit/hyperactivity disorder adverse childhood experiences developmental psychopathology gene-environment correlation intelligence polygenic score Index. décimale : PER Périodiques Résumé : BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) and lower cognitive ability have been linked with increased likelihood of exposure to adversity. We hypothesized that these associations may be partly due to genetic factors. METHODS: We calculated polygenic scores for ADHD and intelligence and assessed psychopathology and general cognitive ability in a sample of 297 youth aged 5-27 years enriched for offspring of parents with mood and psychotic disorders. We calculated an adversity score as a mean of 10 indicators, including socio-economic disadvantage, childhood maltreatment and bullying. We tested the effects of polygenic scores, externalizing symptoms and IQ on adversity scores using mixed-effects linear regression. RESULTS: Externalizing symptoms and general cognitive ability showed expected positive and negative relationships with adversity, respectively. Polygenic scores for intelligence were unrelated to adversity, but polygenic scores for ADHD were associated with adversity (beta = 0.23, 95% CI 0.13 to 0.34, p < .0001). ADHD polygenic scores uniquely explained 4.0% of variance in adversity score. The relationship between polygenic scores for ADHD and adversity was independently significant among individuals with (beta = 0.49, 95% CI 0.25 to 0.75, p < .0001) and without (beta = 0.14, 95% CI 0.02 to 0.26, p = .022) ADHD. CONCLUSIONS: A genetic score indexing liability to ADHD was associated with exposure to adversity in early life. Previously observed associations between externalizing symptoms, lower cognitive ability and adversity may be partially attributed to genetic liability to ADHD. En ligne : http://dx.doi.org/10.1111/jcpp.13159 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=422
in Journal of Child Psychology and Psychiatry > 61-5 (May 2020) . - p.536-544[article] Neurodevelopmental and genetic determinants of exposure to adversity among youth at risk for mental illness [Texte imprimé et/ou numérique] / Alyson ZWICKER, Auteur ; Lynn E. MACKENZIE, Auteur ; Vladislav DROBININ, Auteur ; Amina M. BAGHER, Auteur ; Emily HOWES VALLIS, Auteur ; Lukas PROPPER, Auteur ; Alexa BAGNELL, Auteur ; Sabina ABIDI, Auteur ; Barbara PAVLOVA, Auteur ; Martin ALDA, Auteur ; Eileen M. DENOVAN-WRIGHT, Auteur ; Rudolf UHER, Auteur . - p.536-544.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 61-5 (May 2020) . - p.536-544
Mots-clés : Attention-deficit/hyperactivity disorder adverse childhood experiences developmental psychopathology gene-environment correlation intelligence polygenic score Index. décimale : PER Périodiques Résumé : BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) and lower cognitive ability have been linked with increased likelihood of exposure to adversity. We hypothesized that these associations may be partly due to genetic factors. METHODS: We calculated polygenic scores for ADHD and intelligence and assessed psychopathology and general cognitive ability in a sample of 297 youth aged 5-27 years enriched for offspring of parents with mood and psychotic disorders. We calculated an adversity score as a mean of 10 indicators, including socio-economic disadvantage, childhood maltreatment and bullying. We tested the effects of polygenic scores, externalizing symptoms and IQ on adversity scores using mixed-effects linear regression. RESULTS: Externalizing symptoms and general cognitive ability showed expected positive and negative relationships with adversity, respectively. Polygenic scores for intelligence were unrelated to adversity, but polygenic scores for ADHD were associated with adversity (beta = 0.23, 95% CI 0.13 to 0.34, p < .0001). ADHD polygenic scores uniquely explained 4.0% of variance in adversity score. The relationship between polygenic scores for ADHD and adversity was independently significant among individuals with (beta = 0.49, 95% CI 0.25 to 0.75, p < .0001) and without (beta = 0.14, 95% CI 0.02 to 0.26, p = .022) ADHD. CONCLUSIONS: A genetic score indexing liability to ADHD was associated with exposure to adversity in early life. Previously observed associations between externalizing symptoms, lower cognitive ability and adversity may be partially attributed to genetic liability to ADHD. En ligne : http://dx.doi.org/10.1111/jcpp.13159 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=422 Analysis of common genetic variation and rare CNVs in the Australian Autism Biobank / Chloe X. YAP in Molecular Autism, 12 (2021)
[article]
Titre : Analysis of common genetic variation and rare CNVs in the Australian Autism Biobank Type de document : Texte imprimé et/ou numérique Auteurs : Chloe X. YAP, Auteur ; Gail A. ALVARES, Auteur ; Anjali K. HENDERS, Auteur ; Tian LIN, Auteur ; Leanne WALLACE, Auteur ; Alaina FARRELLY, Auteur ; Tiana MCLAREN, Auteur ; Jolene BERRY, Auteur ; Anna A. E. VINKHUYZEN, Auteur ; Maciej TRZASKOWSKI, Auteur ; Jian ZENG, Auteur ; Yuanhao YANG, Auteur ; Dominique CLEARY, Auteur ; Rachel GROVE, Auteur ; Claire HAFEKOST, Auteur ; Alexis HARUN, Auteur ; Helen HOLDSWORTH, Auteur ; Rachel JELLETT, Auteur ; Feroza KHAN, Auteur ; Lauren LAWSON, Auteur ; Jodie LESLIE, Auteur ; Mira LEVIS FRENK, Auteur ; Anne MASI, Auteur ; Nisha E. MATHEW, Auteur ; Melanie MUNIANDY, Auteur ; Michaela NOTHARD, Auteur ; Peter M. VISSCHER, Auteur ; Paul A. DAWSON, Auteur ; Cheryl DISSANAYAKE, Auteur ; Valsamma EAPEN, Auteur ; Helen S. HEUSSLER, Auteur ; Andrew J. O. WHITEHOUSE, Auteur ; Naomi R. WRAY, Auteur ; Jacob GRATTEN, Auteur Article en page(s) : 12p. Langues : Anglais (eng) Mots-clés : Australian autism biobank Autism spectrum disorder Copy number variation Genetics Polygenic score Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is a complex neurodevelopmental condition whose biological basis is yet to be elucidated. The Australian Autism Biobank (AAB) is an initiative of the Cooperative Research Centre for Living with Autism (Autism CRC) to establish an Australian resource of biospecimens, phenotypes and genomic data for research on autism. METHODS: Genome-wide single-nucleotide polymorphism genotypes were available for 2,477 individuals (after quality control) from 546 families (436 complete), including 886 participants aged 2 to 17 years with diagnosed (n?=?871) or suspected (n?=?15) ASD, 218 siblings without ASD, 1,256 parents, and 117 unrelated children without an ASD diagnosis. The genetic data were used to confirm familial relationships and assign ancestry, which was majority European (n?=?1,964 European individuals). We generated polygenic scores (PGS) for ASD, IQ, chronotype and height in the subset of Europeans, and in 3,490 unrelated ancestry-matched participants from the UK Biobank. We tested for group differences for each PGS, and performed prediction analyses for related phenotypes in the AAB. We called copy-number variants (CNVs) in all participants, and intersected these with high-confidence ASD- and intellectual disability (ID)-associated CNVs and genes from the public domain. RESULTS: The ASD (p?=?6.1e-13), sibling (p?=?4.9e-3) and unrelated (p?=?3.0e-3) groups had significantly higher ASD PGS than UK Biobank controls, whereas this was not the case for height-a control trait. The IQ PGS was a significant predictor of measured IQ in undiagnosed children (r?=?0.24, p?=?2.1e-3) and parents (r?=?0.17, p?=?8.0e-7; 4.0% of variance), but not the ASD group. Chronotype PGS predicted sleep disturbances within the ASD group (r?=?0.13, p?=?1.9e-3; 1.3% of variance). In the CNV analysis, we identified 13 individuals with CNVs overlapping ASD/ID-associated CNVs, and 12 with CNVs overlapping ASD/ID/developmental delay-associated genes identified on the basis of de novo variants. LIMITATIONS: This dataset is modest in size, and the publicly-available genome-wide-association-study (GWAS) summary statistics used to calculate PGS for ASD and other traits are relatively underpowered. CONCLUSIONS: We report on common genetic variation and rare CNVs within the AAB. Prediction analyses using currently available GWAS summary statistics are largely consistent with expected relationships based on published studies. As the size of publicly-available GWAS summary statistics grows, the phenotypic depth of the AAB dataset will provide many opportunities for analyses of autism profiles and co-occurring conditions, including when integrated with other omics datasets generated from AAB biospecimens (blood, urine, stool, hair). En ligne : http://dx.doi.org/10.1186/s13229-020-00407-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=442
in Molecular Autism > 12 (2021) . - 12p.[article] Analysis of common genetic variation and rare CNVs in the Australian Autism Biobank [Texte imprimé et/ou numérique] / Chloe X. YAP, Auteur ; Gail A. ALVARES, Auteur ; Anjali K. HENDERS, Auteur ; Tian LIN, Auteur ; Leanne WALLACE, Auteur ; Alaina FARRELLY, Auteur ; Tiana MCLAREN, Auteur ; Jolene BERRY, Auteur ; Anna A. E. VINKHUYZEN, Auteur ; Maciej TRZASKOWSKI, Auteur ; Jian ZENG, Auteur ; Yuanhao YANG, Auteur ; Dominique CLEARY, Auteur ; Rachel GROVE, Auteur ; Claire HAFEKOST, Auteur ; Alexis HARUN, Auteur ; Helen HOLDSWORTH, Auteur ; Rachel JELLETT, Auteur ; Feroza KHAN, Auteur ; Lauren LAWSON, Auteur ; Jodie LESLIE, Auteur ; Mira LEVIS FRENK, Auteur ; Anne MASI, Auteur ; Nisha E. MATHEW, Auteur ; Melanie MUNIANDY, Auteur ; Michaela NOTHARD, Auteur ; Peter M. VISSCHER, Auteur ; Paul A. DAWSON, Auteur ; Cheryl DISSANAYAKE, Auteur ; Valsamma EAPEN, Auteur ; Helen S. HEUSSLER, Auteur ; Andrew J. O. WHITEHOUSE, Auteur ; Naomi R. WRAY, Auteur ; Jacob GRATTEN, Auteur . - 12p.
Langues : Anglais (eng)
in Molecular Autism > 12 (2021) . - 12p.
Mots-clés : Australian autism biobank Autism spectrum disorder Copy number variation Genetics Polygenic score Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is a complex neurodevelopmental condition whose biological basis is yet to be elucidated. The Australian Autism Biobank (AAB) is an initiative of the Cooperative Research Centre for Living with Autism (Autism CRC) to establish an Australian resource of biospecimens, phenotypes and genomic data for research on autism. METHODS: Genome-wide single-nucleotide polymorphism genotypes were available for 2,477 individuals (after quality control) from 546 families (436 complete), including 886 participants aged 2 to 17 years with diagnosed (n?=?871) or suspected (n?=?15) ASD, 218 siblings without ASD, 1,256 parents, and 117 unrelated children without an ASD diagnosis. The genetic data were used to confirm familial relationships and assign ancestry, which was majority European (n?=?1,964 European individuals). We generated polygenic scores (PGS) for ASD, IQ, chronotype and height in the subset of Europeans, and in 3,490 unrelated ancestry-matched participants from the UK Biobank. We tested for group differences for each PGS, and performed prediction analyses for related phenotypes in the AAB. We called copy-number variants (CNVs) in all participants, and intersected these with high-confidence ASD- and intellectual disability (ID)-associated CNVs and genes from the public domain. RESULTS: The ASD (p?=?6.1e-13), sibling (p?=?4.9e-3) and unrelated (p?=?3.0e-3) groups had significantly higher ASD PGS than UK Biobank controls, whereas this was not the case for height-a control trait. The IQ PGS was a significant predictor of measured IQ in undiagnosed children (r?=?0.24, p?=?2.1e-3) and parents (r?=?0.17, p?=?8.0e-7; 4.0% of variance), but not the ASD group. Chronotype PGS predicted sleep disturbances within the ASD group (r?=?0.13, p?=?1.9e-3; 1.3% of variance). In the CNV analysis, we identified 13 individuals with CNVs overlapping ASD/ID-associated CNVs, and 12 with CNVs overlapping ASD/ID/developmental delay-associated genes identified on the basis of de novo variants. LIMITATIONS: This dataset is modest in size, and the publicly-available genome-wide-association-study (GWAS) summary statistics used to calculate PGS for ASD and other traits are relatively underpowered. CONCLUSIONS: We report on common genetic variation and rare CNVs within the AAB. Prediction analyses using currently available GWAS summary statistics are largely consistent with expected relationships based on published studies. As the size of publicly-available GWAS summary statistics grows, the phenotypic depth of the AAB dataset will provide many opportunities for analyses of autism profiles and co-occurring conditions, including when integrated with other omics datasets generated from AAB biospecimens (blood, urine, stool, hair). En ligne : http://dx.doi.org/10.1186/s13229-020-00407-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=442 Evaluating chronic emotional dysregulation and irritability in relation to ADHD and depression genetic risk in children with ADHD / Joel T. NIGG in Journal of Child Psychology and Psychiatry, 61-2 (February 2020)
[article]
Titre : Evaluating chronic emotional dysregulation and irritability in relation to ADHD and depression genetic risk in children with ADHD Type de document : Texte imprimé et/ou numérique Auteurs : Joel T. NIGG, Auteur ; Sarah L. KARALUNAS, Auteur ; Hanna C. GUSTAFSSON, Auteur ; Priya BHATT, Auteur ; Peter RYABININ, Auteur ; Michael A. MOONEY, Auteur ; Stephen V. FARAONE, Auteur ; Damien A. FAIR, Auteur ; Beth WILMOT, Auteur Article en page(s) : p.205-214 Langues : Anglais (eng) Mots-clés : Adhd irritability polygenic score temperament Index. décimale : PER Périodiques Résumé : BACKGROUND: A central nosological problem concerns the etiological relationship of emotional dysregulation with ADHD. Molecular genetic risk scores provide a novel method for informing this question. METHODS: Participants were 514 community-recruited children of Northern European descent age 7-11 defined as ADHD or non-ADHD by detailed research evaluation. Parents-rated ADHD on standardized ratings and child temperament on the Temperament in Middle Childhood Questionnaire (TMCQ) and reported on ADHD and comorbid disorders by semi-structured clinical interview. Categorical and dimensional variables were created for ADHD, emotional dysregulation (implicating disruption of regulation of both anger-irritability and of positive valence surgency-sensation seeking), and irritability alone (anger dysregulation). Genome-wide polygenic risk scores (PRS) were computed for ADHD and depression genetic liability. Structural equation models and computationally derived emotion profiles guided analysis. RESULTS: The ADHD PRS was associated in variable-centered analyses with irritability (beta = .179, 95% CI = 0.087-0.280; DeltaR(2) = .034, p < .0002), but also with surgency/sensation seeking (B = .146, 95%CI = 0.052-0.240, DeltaR(2) =.022, p = .002). In person-centered analysis, the ADHD PRS was elevated in the emotion dysregulation ADHD group versus other ADHD children (OR = 1.44, 95% CI = 1.03-2.20, Nagelkerke DeltaR(2) = .013, p = .033) but did not differentiate irritable from surgent ADHD profiles. All effects were independent of variation in ADHD severity across traits or groups. The depression PRS was related to oppositional defiant disorder but not to ADHD emotion dysregulation. CONCLUSIONS: Irritability-anger and surgency-sensation seeking, as forms of negative and positively valenced dysregulated affect in ADHD populations, both relate principally to ADHD genetic risk and not mood-related genetic risk. En ligne : http://dx.doi.org/10.1111/jcpp.13132 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=415
in Journal of Child Psychology and Psychiatry > 61-2 (February 2020) . - p.205-214[article] Evaluating chronic emotional dysregulation and irritability in relation to ADHD and depression genetic risk in children with ADHD [Texte imprimé et/ou numérique] / Joel T. NIGG, Auteur ; Sarah L. KARALUNAS, Auteur ; Hanna C. GUSTAFSSON, Auteur ; Priya BHATT, Auteur ; Peter RYABININ, Auteur ; Michael A. MOONEY, Auteur ; Stephen V. FARAONE, Auteur ; Damien A. FAIR, Auteur ; Beth WILMOT, Auteur . - p.205-214.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 61-2 (February 2020) . - p.205-214
Mots-clés : Adhd irritability polygenic score temperament Index. décimale : PER Périodiques Résumé : BACKGROUND: A central nosological problem concerns the etiological relationship of emotional dysregulation with ADHD. Molecular genetic risk scores provide a novel method for informing this question. METHODS: Participants were 514 community-recruited children of Northern European descent age 7-11 defined as ADHD or non-ADHD by detailed research evaluation. Parents-rated ADHD on standardized ratings and child temperament on the Temperament in Middle Childhood Questionnaire (TMCQ) and reported on ADHD and comorbid disorders by semi-structured clinical interview. Categorical and dimensional variables were created for ADHD, emotional dysregulation (implicating disruption of regulation of both anger-irritability and of positive valence surgency-sensation seeking), and irritability alone (anger dysregulation). Genome-wide polygenic risk scores (PRS) were computed for ADHD and depression genetic liability. Structural equation models and computationally derived emotion profiles guided analysis. RESULTS: The ADHD PRS was associated in variable-centered analyses with irritability (beta = .179, 95% CI = 0.087-0.280; DeltaR(2) = .034, p < .0002), but also with surgency/sensation seeking (B = .146, 95%CI = 0.052-0.240, DeltaR(2) =.022, p = .002). In person-centered analysis, the ADHD PRS was elevated in the emotion dysregulation ADHD group versus other ADHD children (OR = 1.44, 95% CI = 1.03-2.20, Nagelkerke DeltaR(2) = .013, p = .033) but did not differentiate irritable from surgent ADHD profiles. All effects were independent of variation in ADHD severity across traits or groups. The depression PRS was related to oppositional defiant disorder but not to ADHD emotion dysregulation. CONCLUSIONS: Irritability-anger and surgency-sensation seeking, as forms of negative and positively valenced dysregulated affect in ADHD populations, both relate principally to ADHD genetic risk and not mood-related genetic risk. En ligne : http://dx.doi.org/10.1111/jcpp.13132 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=415 Genetic risk of AUDs and childhood impulsivity: Examining the role of parenting and family environment / Jinni SU in Development and Psychopathology, 34-5 (December 2022)
[article]
Titre : Genetic risk of AUDs and childhood impulsivity: Examining the role of parenting and family environment Type de document : Texte imprimé et/ou numérique Auteurs : Jinni SU, Auteur ; Angel TREVINO, Auteur ; Belal JAMIL, Auteur ; Fazil ALIEV, Auteur Article en page(s) : p.1827-1840 Langues : Anglais (eng) Mots-clés : alcohol family conflict impulsivity parenting polygenic score Index. décimale : PER Périodiques Résumé : This study examined the independent and interactive effects of genetic risk for alcohol use disorder (AUD), parenting behaviors, and family environment on childhood impulsivity. Data were drawn from White (n = 5,991), Black/African American (n = 1,693), and Hispanic/Latino (n = 2,118) youth who completed the baseline assessment (age 9 “10) and had genotypic data available from the Adolescent Brain Cognitive Development Study. Participants completed questionnaires and provided saliva or blood samples for genotyping. Results indicated no significant main effects of AUD genome-wide polygenic scores (AUD-PRS) on childhood impulsivity as measured by the UPPS-P scale across racial/ethnic groups. In general, parental monitoring and parental acceptance were associated with lower impulsivity; family conflict was associated with higher impulsivity. There was an interaction effect between AUD-PRS and family conflict, such that family conflict exacerbated the association between AUD-PRS and positive urgency, only among Black/African American youth. This was the only significant interaction effect detected from a total of 45 tests (five impulsivity dimensions, three subsamples, and three family factors), and thus may be a false positive and needs to be replicated. These findings highlight the important role of parenting behaviors and family conflict in relation to impulsivity among children. En ligne : http://dx.doi.org/10.1017/S095457942200092X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=492
in Development and Psychopathology > 34-5 (December 2022) . - p.1827-1840[article] Genetic risk of AUDs and childhood impulsivity: Examining the role of parenting and family environment [Texte imprimé et/ou numérique] / Jinni SU, Auteur ; Angel TREVINO, Auteur ; Belal JAMIL, Auteur ; Fazil ALIEV, Auteur . - p.1827-1840.
Langues : Anglais (eng)
in Development and Psychopathology > 34-5 (December 2022) . - p.1827-1840
Mots-clés : alcohol family conflict impulsivity parenting polygenic score Index. décimale : PER Périodiques Résumé : This study examined the independent and interactive effects of genetic risk for alcohol use disorder (AUD), parenting behaviors, and family environment on childhood impulsivity. Data were drawn from White (n = 5,991), Black/African American (n = 1,693), and Hispanic/Latino (n = 2,118) youth who completed the baseline assessment (age 9 “10) and had genotypic data available from the Adolescent Brain Cognitive Development Study. Participants completed questionnaires and provided saliva or blood samples for genotyping. Results indicated no significant main effects of AUD genome-wide polygenic scores (AUD-PRS) on childhood impulsivity as measured by the UPPS-P scale across racial/ethnic groups. In general, parental monitoring and parental acceptance were associated with lower impulsivity; family conflict was associated with higher impulsivity. There was an interaction effect between AUD-PRS and family conflict, such that family conflict exacerbated the association between AUD-PRS and positive urgency, only among Black/African American youth. This was the only significant interaction effect detected from a total of 45 tests (five impulsivity dimensions, three subsamples, and three family factors), and thus may be a false positive and needs to be replicated. These findings highlight the important role of parenting behaviors and family conflict in relation to impulsivity among children. En ligne : http://dx.doi.org/10.1017/S095457942200092X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=492 Look duration at the face as a developmental endophenotype: elucidating pathways to autism and ADHD / Anna GUI in Development and Psychopathology, 32-4 (October 2020)
PermalinkThe role of parental genotype in the intergenerational transmission of externalizing behavior: Evidence for genetic nurturance / Sally I. Chun KUO in Development and Psychopathology, 34-5 (December 2022)
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