Evaluating the interrelations between the autism polygenic score and psychiatric family history in risk for autism / Diana SCHENDEL in Autism Research, 15-1 (January 2022)  

Public ISBD [article]  inAutism Research > 15-1 (January 2022) . - p.171-182 Titre : Evaluating the interrelations between the autism polygenic score and psychiatric family history in risk for autism Type de document : Texte imprimé et/ou numérique Auteurs : Diana SCHENDEL, Auteur ; T. MUNK LAURSEN, Auteur ; C. ALBIÑANA, Auteur ; B. VILHJALMSSON, Auteur ; Christine LADD-ACOSTA, Auteur ; M. D. FALLIN, Auteur ; Kelly S. BENKE, Auteur ; B. LEE, Auteur ; J. GROVE, Auteur ; Amy E. KALKBRENNER, Auteur ; L. EJLSKOV, Auteur ; D. HOUGAARD, Auteur ; Jonas BYBJERG-GRAUHOLM, Auteur ; M. BAEKVAD-HANSEN, Auteur ; A. D. BØRGLUM, Auteur ; T. WERGE, Auteur ; M. NORDENTOFT, Auteur ; P. B. MORTENSEN, Auteur ; E. AGERBO, Auteur Article en page(s) : p.171-182 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/genetics  Autistic Disorder/genetics  Case-Control Studies  Humans  Multifactorial Inheritance/genetics  Risk Factors  Siblings  autism spectrum disorder  case-control studies  family history  genetic risk factors  polygenic risk score Index. décimale : PER Périodiques Résumé : Psychiatric family history or a high autism polygenic risk score (PRS) have been separately linked to autism spectrum disorder (ASD) risk. The study aimed to simultaneously consider psychiatric family history and individual autism genetic liability (PRS) in autism risk. We performed a case-control study of all Denmark singleton births, May 1981-December 2005, in Denmark at their first birthday and a known mother. Cases were diagnosed with ASD before 2013 and controls comprised a random sample of 30,000 births without ASD, excluding persons with non-Denmark-born parents, missing ASD PRS, non-European ancestry. Adjusted odds ratios (aOR) were estimated for ASD by PRS decile and by psychiatric history in parents or full siblings (8 mutually-exclusive categories) using logistic regression. Adjusted ASD PRS z-score least-squares means were estimated by psychiatric family history category. ASD risk (11,339 ASD cases; 20,175 controls) from ASD PRS was not substantially altered after accounting for psychiatric family history (e.g., ASD PRS 10th decile aOR: 2.35 (95% CI 2.11-2.63) before vs 2.11 (95% CI 1.91-2.40) after adjustment) nor from psychiatric family history after accounting for ASD PRS (e.g., ASD family history aOR: 6.73 (95% CI 5.89-7.68) before vs 6.32 (95% CI 5.53-7.22) after adjustment). ASD risk from ASD PRS varied slightly by psychiatric family history. While ASD risk from psychiatric family history was not accounted for by ASD PRS and vice versa, risk overlap between the two factors will likely increase as measures of genetic risk improve. The two factors are best viewed as complementary measures of family-based autism risk. LAY SUMMARY: Autism risk from a history of mental disorders in the immediate family was not explained by a measure of individual genetic risk (autism polygenic risk score) and vice versa. That is, genetic risk did not appear to overlap family history risk. As genetic measures for autism improve then the overlap in autism risk from family history versus genetic factors will likely increase, but further study may be needed to fully determine the components of risk and how they are inter-related between these key family factors. Meanwhile, the two factors may be best viewed as complementary measures of autism family-based risk. En ligne : http://dx.doi.org/10.1002/aur.2629 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450 [article] Evaluating the interrelations between the autism polygenic score and psychiatric family history in risk for autism [Texte imprimé et/ou numérique] / Diana SCHENDEL, Auteur ; T. MUNK LAURSEN, Auteur ; C. ALBIÑANA, Auteur ; B. VILHJALMSSON, Auteur ; Christine LADD-ACOSTA, Auteur ; M. D. FALLIN, Auteur ; Kelly S. BENKE, Auteur ; B. LEE, Auteur ; J. GROVE, Auteur ; Amy E. KALKBRENNER, Auteur ; L. EJLSKOV, Auteur ; D. HOUGAARD, Auteur ; Jonas BYBJERG-GRAUHOLM, Auteur ; M. BAEKVAD-HANSEN, Auteur ; A. D. BØRGLUM, Auteur ; T. WERGE, Auteur ; M. NORDENTOFT, Auteur ; P. B. MORTENSEN, Auteur ; E. AGERBO, Auteur . - p.171-182. Langues : Anglais (eng) in Autism Research > 15-1 (January 2022) . - p.171-182 Mots-clés : Autism Spectrum Disorder/genetics  Autistic Disorder/genetics  Case-Control Studies  Humans  Multifactorial Inheritance/genetics  Risk Factors  Siblings  autism spectrum disorder  case-control studies  family history  genetic risk factors  polygenic risk score Index. décimale : PER Périodiques Résumé : Psychiatric family history or a high autism polygenic risk score (PRS) have been separately linked to autism spectrum disorder (ASD) risk. The study aimed to simultaneously consider psychiatric family history and individual autism genetic liability (PRS) in autism risk. We performed a case-control study of all Denmark singleton births, May 1981-December 2005, in Denmark at their first birthday and a known mother. Cases were diagnosed with ASD before 2013 and controls comprised a random sample of 30,000 births without ASD, excluding persons with non-Denmark-born parents, missing ASD PRS, non-European ancestry. Adjusted odds ratios (aOR) were estimated for ASD by PRS decile and by psychiatric history in parents or full siblings (8 mutually-exclusive categories) using logistic regression. Adjusted ASD PRS z-score least-squares means were estimated by psychiatric family history category. ASD risk (11,339 ASD cases; 20,175 controls) from ASD PRS was not substantially altered after accounting for psychiatric family history (e.g., ASD PRS 10th decile aOR: 2.35 (95% CI 2.11-2.63) before vs 2.11 (95% CI 1.91-2.40) after adjustment) nor from psychiatric family history after accounting for ASD PRS (e.g., ASD family history aOR: 6.73 (95% CI 5.89-7.68) before vs 6.32 (95% CI 5.53-7.22) after adjustment). ASD risk from ASD PRS varied slightly by psychiatric family history. While ASD risk from psychiatric family history was not accounted for by ASD PRS and vice versa, risk overlap between the two factors will likely increase as measures of genetic risk improve. The two factors are best viewed as complementary measures of family-based autism risk. LAY SUMMARY: Autism risk from a history of mental disorders in the immediate family was not explained by a measure of individual genetic risk (autism polygenic risk score) and vice versa. That is, genetic risk did not appear to overlap family history risk. As genetic measures for autism improve then the overlap in autism risk from family history versus genetic factors will likely increase, but further study may be needed to fully determine the components of risk and how they are inter-related between these key family factors. Meanwhile, the two factors may be best viewed as complementary measures of autism family-based risk. En ligne : http://dx.doi.org/10.1002/aur.2629 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450

Polygenic and environmental influences on the course of African Americans' alcohol use from early adolescence through young adulthood / Jill A. RABINOWITZ in Development and Psychopathology, 32-2 (May 2020)  

Public ISBD [article]  inDevelopment and Psychopathology > 32-2 (May 2020) . - p.703-718 Titre : Polygenic and environmental influences on the course of African Americans' alcohol use from early adolescence through young adulthood Type de document : Texte imprimé et/ou numérique Auteurs : Jill A. RABINOWITZ, Auteur ; Rashelle J. MUSCI, Auteur ; Beth REBOUSSIN, Auteur ; Adam J. MILAM, Auteur ; Kelly S. BENKE, Auteur ; George R. UHL, Auteur ; Danielle Y. SISTO, Auteur ; Nicholas S. IALONGO, Auteur ; Brion S. MAHER, Auteur Article en page(s) : p.703-718 Langues : Anglais (eng) Mots-clés : alcohol use classes  antisocial behavior polygenic risk score  community disadvantage  internalizing symptoms polygenic risk score  parental monitoring Index. décimale : PER Périodiques Résumé : The study examined (a) whether alcohol use subgroups could be identified among African Americans assessed from adolescence through early adulthood, and (b) whether subgroup membership was associated with the interaction between internalizing symptoms and antisocial behavior polygenic risk scores (PRSs) and environmental characteristics (i.e., parental monitoring, community disadvantage). Participants (N = 436) were initially recruited for an elementary school-based prevention trial in a Mid-Atlantic city. Youths reported on the frequency of their past year alcohol use from ages 14-26. DNA was obtained from participants at age 21. Internalizing symptoms and antisocial behavior PRSs were created based on a genome-wide association study (GWAS) conducted by Benke et al. (2014) and Tielbeek et al. (2017), respectively. Parental monitoring and community disadvantage were assessed at age 12. Four classes of past year alcohol use were identified: (a) early-onset, increasing; (b) late-onset, moderate use; (c) low steady; and (d) early-onset, decreasing. In high community disadvantaged settings, participants with a higher internalizing symptoms PRS were more likely to be in the early-onset, decreasing class than the low steady class. When exposed to elevated community disadvantage, participants with a higher antisocial behavior PRS were more likely to be in the early-onset, increasing class than the early-onset, decreasing and late-onset, moderate use classes. En ligne : http://dx.doi.org/10.1017/s0954579419000701 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=426 [article] Polygenic and environmental influences on the course of African Americans' alcohol use from early adolescence through young adulthood [Texte imprimé et/ou numérique] / Jill A. RABINOWITZ, Auteur ; Rashelle J. MUSCI, Auteur ; Beth REBOUSSIN, Auteur ; Adam J. MILAM, Auteur ; Kelly S. BENKE, Auteur ; George R. UHL, Auteur ; Danielle Y. SISTO, Auteur ; Nicholas S. IALONGO, Auteur ; Brion S. MAHER, Auteur . - p.703-718. Langues : Anglais (eng) in Development and Psychopathology > 32-2 (May 2020) . - p.703-718 Mots-clés : alcohol use classes  antisocial behavior polygenic risk score  community disadvantage  internalizing symptoms polygenic risk score  parental monitoring Index. décimale : PER Périodiques Résumé : The study examined (a) whether alcohol use subgroups could be identified among African Americans assessed from adolescence through early adulthood, and (b) whether subgroup membership was associated with the interaction between internalizing symptoms and antisocial behavior polygenic risk scores (PRSs) and environmental characteristics (i.e., parental monitoring, community disadvantage). Participants (N = 436) were initially recruited for an elementary school-based prevention trial in a Mid-Atlantic city. Youths reported on the frequency of their past year alcohol use from ages 14-26. DNA was obtained from participants at age 21. Internalizing symptoms and antisocial behavior PRSs were created based on a genome-wide association study (GWAS) conducted by Benke et al. (2014) and Tielbeek et al. (2017), respectively. Parental monitoring and community disadvantage were assessed at age 12. Four classes of past year alcohol use were identified: (a) early-onset, increasing; (b) late-onset, moderate use; (c) low steady; and (d) early-onset, decreasing. In high community disadvantaged settings, participants with a higher internalizing symptoms PRS were more likely to be in the early-onset, decreasing class than the low steady class. When exposed to elevated community disadvantage, participants with a higher antisocial behavior PRS were more likely to be in the early-onset, increasing class than the early-onset, decreasing and late-onset, moderate use classes. En ligne : http://dx.doi.org/10.1017/s0954579419000701 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=426

The effects of the interplay of genetics and early environmental risk on the course of internalizing symptoms from late childhood through adolescence / Rashelle J. MUSCI in Development and Psychopathology, 28-1 (February 2016)  

Public ISBD [article]  inDevelopment and Psychopathology > 28-1 (February 2016) . - p.225-237 Titre : The effects of the interplay of genetics and early environmental risk on the course of internalizing symptoms from late childhood through adolescence Type de document : Texte imprimé et/ou numérique Auteurs : Rashelle J. MUSCI, Auteur ; Katherine E. MASYN, Auteur ; Kelly S. BENKE, Auteur ; Brion MAHER, Auteur ; George UHL, Auteur ; Nicholas S. IALONGO, Auteur Article en page(s) : p.225-237 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Internalizing symptoms during adolescence and beyond is a major public health concern, particularly because severe symptoms can lead to the diagnosis of a number of serious psychiatric conditions. This study utilizes a unique sample with a complex statistical method in order to explore Gene × Environment interactions found in internalizing symptoms during adolescence. Data for this study were drawn from a longitudinal prevention intervention study (n = 798) of Baltimore city school children. Internalizing symptom data were collected using self-report and blood or saliva samples genotyped using Affymetrix 6.0 microarrays. A major depression polygenic score was created for each individual using information from the major depressive disorder Psychiatric Genetics Consortium and used as a predictor in a latent trait–state–occasion model. The major depressive disorder polygenic score was a significant predictor of the stable latent trait variable, which captures time-independent phenotypic variability. In addition, an early childhood stressor of death or divorce was a significant predictor of occasion-specific variables. A Gene × Environment interaction was not a significant predictor of the latent trait or occasion variables. These findings support the importance of genetics on the stable latent trait portion of internalizing symptoms across adolescence. En ligne : http://dx.doi.org/10.1017/S0954579415000401 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=278 [article] The effects of the interplay of genetics and early environmental risk on the course of internalizing symptoms from late childhood through adolescence [Texte imprimé et/ou numérique] / Rashelle J. MUSCI, Auteur ; Katherine E. MASYN, Auteur ; Kelly S. BENKE, Auteur ; Brion MAHER, Auteur ; George UHL, Auteur ; Nicholas S. IALONGO, Auteur . - p.225-237. Langues : Anglais (eng) in Development and Psychopathology > 28-1 (February 2016) . - p.225-237 Index. décimale : PER Périodiques Résumé : Internalizing symptoms during adolescence and beyond is a major public health concern, particularly because severe symptoms can lead to the diagnosis of a number of serious psychiatric conditions. This study utilizes a unique sample with a complex statistical method in order to explore Gene × Environment interactions found in internalizing symptoms during adolescence. Data for this study were drawn from a longitudinal prevention intervention study (n = 798) of Baltimore city school children. Internalizing symptom data were collected using self-report and blood or saliva samples genotyped using Affymetrix 6.0 microarrays. A major depression polygenic score was created for each individual using information from the major depressive disorder Psychiatric Genetics Consortium and used as a predictor in a latent trait–state–occasion model. The major depressive disorder polygenic score was a significant predictor of the stable latent trait variable, which captures time-independent phenotypic variability. In addition, an early childhood stressor of death or divorce was a significant predictor of occasion-specific variables. A Gene × Environment interaction was not a significant predictor of the latent trait or occasion variables. These findings support the importance of genetics on the stable latent trait portion of internalizing symptoms across adolescence. En ligne : http://dx.doi.org/10.1017/S0954579415000401 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=278

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