14 recherche sur le mot-clé 'polygenic risk score'

Editorial Perspective: From schizophrenia polygenic risk score to vulnerability (endo-)phenotypes: translational pathways in child and adolescent mental health / Michele POLETTI in Journal of Child Psychology and Psychiatry, 59-7 (July 2018)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 59-7 (July 2018) . - p.822-825 Titre : Editorial Perspective: From schizophrenia polygenic risk score to vulnerability (endo-)phenotypes: translational pathways in child and adolescent mental health Type de document : texte imprimé Auteurs : Michele POLETTI, Auteur ; Andrea RABALLO, Auteur Article en page(s) : p.822-825 Langues : Anglais (eng) Mots-clés : Schizophrenia  development  phenotype  polygenic risk score  psychopathology  vulnerability Index. décimale : PER Périodiques Résumé : The Polygenic Risk Scores (PRS) approach is becoming increasingly prominent in psycho-behavioral research, however, its translational potential is still relatively underconceptualized. Indeed, PRS paradigm (which capitalizes on the combination of multiple genetic markers into a single proxy score to predict lifetime outcomes) has the potential to unravel some of the developmental complexities leading to severe mental disorders. With respect to schizophrenia, the application of PRS approach to child-adolescent cohorts from the general population, provides a crucial vantage point for understanding how presumed genetic predisposition is manifested during developmental years. Clearly, this is essential for etiological research as well as for the timely identification of the earliest stages of those specific psychopathological trajectories leading to psychosis. Therefore, the translational import of the PRS approach could improve our etiopathogenetic understanding of schizophrenia (e.g., allowing the disentanglement of the respective contribution of genetic and environmental risk factors along neurodevelopment) and further refine current staging models for early detection of vulnerability to psychosis (e.g., providing the rationale for more developmentally oriented reformulations of clinical high-risk criteria). En ligne : http://dx.doi.org/10.1111/jcpp.12857 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=368 [article] Editorial Perspective: From schizophrenia polygenic risk score to vulnerability (endo-)phenotypes: translational pathways in child and adolescent mental health [texte imprimé] / Michele POLETTI, Auteur ; Andrea RABALLO, Auteur . - p.822-825. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 59-7 (July 2018) . - p.822-825 Mots-clés : Schizophrenia  development  phenotype  polygenic risk score  psychopathology  vulnerability Index. décimale : PER Périodiques Résumé : The Polygenic Risk Scores (PRS) approach is becoming increasingly prominent in psycho-behavioral research, however, its translational potential is still relatively underconceptualized. Indeed, PRS paradigm (which capitalizes on the combination of multiple genetic markers into a single proxy score to predict lifetime outcomes) has the potential to unravel some of the developmental complexities leading to severe mental disorders. With respect to schizophrenia, the application of PRS approach to child-adolescent cohorts from the general population, provides a crucial vantage point for understanding how presumed genetic predisposition is manifested during developmental years. Clearly, this is essential for etiological research as well as for the timely identification of the earliest stages of those specific psychopathological trajectories leading to psychosis. Therefore, the translational import of the PRS approach could improve our etiopathogenetic understanding of schizophrenia (e.g., allowing the disentanglement of the respective contribution of genetic and environmental risk factors along neurodevelopment) and further refine current staging models for early detection of vulnerability to psychosis (e.g., providing the rationale for more developmentally oriented reformulations of clinical high-risk criteria). En ligne : http://dx.doi.org/10.1111/jcpp.12857 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=368

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 Auteurs : Diana SCHENDEL, Auteur ; Thomas MUNK LAURSEN, Auteur ; Clara ALBIÑANA, Auteur ; Bjarni VILHJALMSSON, Auteur ; Christine LADD-ACOSTA, Auteur ; M. Daniele FALLIN, Auteur ; Kelly S. BENKE, Auteur ; Brian K. LEE, Auteur ; Jakob GROVE, Auteur ; Amy E. KALKBRENNER, Auteur ; Linda EJLSKOV, Auteur ; David HOUGAARD, Auteur ; Jonas BYBJERG-GRAUHOLM, Auteur ; Marie BAEKVAD-HANSEN, Auteur ; Anders D. BØRGLUM, Auteur ; Thomas WERGE, Auteur ; Merete NORDENTOFT, Auteur ; Preben Bo MORTENSEN, Auteur ; Esben 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] / Diana SCHENDEL, Auteur ; Thomas MUNK LAURSEN, Auteur ; Clara ALBIÑANA, Auteur ; Bjarni VILHJALMSSON, Auteur ; Christine LADD-ACOSTA, Auteur ; M. Daniele FALLIN, Auteur ; Kelly S. BENKE, Auteur ; Brian K. LEE, Auteur ; Jakob GROVE, Auteur ; Amy E. KALKBRENNER, Auteur ; Linda EJLSKOV, Auteur ; David HOUGAARD, Auteur ; Jonas BYBJERG-GRAUHOLM, Auteur ; Marie BAEKVAD-HANSEN, Auteur ; Anders D. BØRGLUM, Auteur ; Thomas WERGE, Auteur ; Merete NORDENTOFT, Auteur ; Preben Bo MORTENSEN, Auteur ; Esben 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

Copy Number Variants and Polygenic Risk Scores Predict Need of Care in Autism and/or ADHD Families / Sonja LABIANCA in Journal of Autism and Developmental Disorders, 51-1 (January 2021)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 51-1 (January 2021) . - p.276-285 Titre : Copy Number Variants and Polygenic Risk Scores Predict Need of Care in Autism and/or ADHD Families Type de document : texte imprimé Auteurs : Sonja LABIANCA, Auteur ; Jette LABIANCA, Auteur ; Anne Katrine PAGSBERG, Auteur ; Klaus Damgaard JAKOBSEN, Auteur ; Vivek APPADURAI, Auteur ; Alfonso BUIL, Auteur ; Thomas WERGE, Auteur Article en page(s) : p.276-285 Langues : Anglais (eng) Mots-clés : Attention deficit/hyperactivity disorder  Autism spectrum disorder  Comorbidity  Copy number variants  Families  Polygenic risk score Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) are highly heritable neurodevelopmental disorders that frequently co-occur. Both rare and common genetic variants are important for ASD and ADHD risk but their combined contribution to clinical heterogeneity is unclear. In a sample of 39 ASD and/or ADHD families we estimated the overall variance explained by known rare copy number variants (CNVs) and polygenic risk score (PRS) from common variants to be 10% in comorbid ASD/ADHD, 4% in ASD and 2% in ADHD. We show that burden of large, rare CNVs and PRS is significantly higher in adult ASD and/or ADHD patients with sustained need for specialist care compared to their unaffected relatives, while affected relatives fall in-between the two. En ligne : http://dx.doi.org/10.1007/s10803-020-04552-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=437 [article] Copy Number Variants and Polygenic Risk Scores Predict Need of Care in Autism and/or ADHD Families [texte imprimé] / Sonja LABIANCA, Auteur ; Jette LABIANCA, Auteur ; Anne Katrine PAGSBERG, Auteur ; Klaus Damgaard JAKOBSEN, Auteur ; Vivek APPADURAI, Auteur ; Alfonso BUIL, Auteur ; Thomas WERGE, Auteur . - p.276-285. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 51-1 (January 2021) . - p.276-285 Mots-clés : Attention deficit/hyperactivity disorder  Autism spectrum disorder  Comorbidity  Copy number variants  Families  Polygenic risk score Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) are highly heritable neurodevelopmental disorders that frequently co-occur. Both rare and common genetic variants are important for ASD and ADHD risk but their combined contribution to clinical heterogeneity is unclear. In a sample of 39 ASD and/or ADHD families we estimated the overall variance explained by known rare copy number variants (CNVs) and polygenic risk score (PRS) from common variants to be 10% in comorbid ASD/ADHD, 4% in ASD and 2% in ADHD. We show that burden of large, rare CNVs and PRS is significantly higher in adult ASD and/or ADHD patients with sustained need for specialist care compared to their unaffected relatives, while affected relatives fall in-between the two. En ligne : http://dx.doi.org/10.1007/s10803-020-04552-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=437

Language deficits in specific language impairment, attention deficit/hyperactivity disorder, and autism spectrum disorder: An analysis of polygenic risk / Ron NUDEL in Autism Research, 13-3 (March 2020)  

Public ISBD [article]  inAutism Research > 13-3 (March 2020) . - p.369-381 Titre : Language deficits in specific language impairment, attention deficit/hyperactivity disorder, and autism spectrum disorder: An analysis of polygenic risk Type de document : texte imprimé Auteurs : Ron NUDEL, Auteur ; Camilla A.J. CHRISTIANI, Auteur ; Jessica OHLAND, Auteur ; Md Jamal UDDIN, Auteur ; Nicoline HEMAGER, Auteur ; Ditte ELLERSGAARD, Auteur ; Katrine S. SPANG, Auteur ; Birgitte K. BURTON, Auteur ; Aja GREVE, Auteur ; Ditte L. GANTRIIS, Auteur ; Jonas BYBJERG-GRAUHOLM, Auteur ; Jens Richardt MØLLEGAARD JEPSEN, Auteur ; Anne A.E. THORUP, Auteur ; Ole MORS, Auteur ; Merete NORDENTOFT, Auteur ; Thomas WERGE, Auteur Article en page(s) : p.369-381 Langues : Anglais (eng) Mots-clés : attention deficit hyperactivity disorder  autism spectrum disorder  genome-wide association study  polygenic risk score  specific language impairment Index. décimale : PER Périodiques Résumé : Language is one of the cognitive domains often impaired across many neurodevelopmental disorders. While for some disorders the linguistic deficit is the primary impairment (e.g., specific language impairment, SLI), for others it may accompany broader behavioral problems (e.g., autism). The precise nature of this phenotypic overlap has been the subject of debate. Moreover, several studies have found genetic overlaps across neurodevelopmental disorders. This raises the question of whether these genetic overlaps may correlate with phenotypic overlaps and, if so, in what manner. Here, we apply a genome-wide approach to the study of the linguistic deficit in SLI, autism spectrum disorder (ASD), and attention deficit/hyperactivity disorder (ADHD). Using a discovery genome-wide association study of SLI, we generate polygenic risk scores (PRS) in an independent sample which includes children with language impairment, SLI, ASD or ADHD and age-matched controls and perform regression analyses across groups. The SLI-trained PRS significantly predicted risk in the SLI case-control group (adjusted R(2) = 6.24%; P = 0.024) but not in the ASD or ADHD case-control groups (adjusted R(2) = 0.0004%, 0.01%; P = 0.984, 0.889, respectively) nor for height, used as a negative control (R(2) = 0.2%; P = 0.452). Additionally, there was a significant difference in the normalized PRS between children with SLI and children with ASD (common language effect size = 0.66; P = 0.044). Our study suggests no additive common-variant genetic overlap between SLI and ASD and ADHD. This is discussed in the context of phenotypic studies of SLI and related disorders. Autism Res 2020, 13: 369-381. (c) 2019 The Authors. Autism Research published by International Society for Autism Research published by Wiley Periodicals, Inc. LAY SUMMARY: Language deficits are characteristic of specific language impairment (SLI), but may also be found in other neurodevelopmental disorders, such as autism spectrum disorder (ASD) and attention deficit/hyperactivity disorder (ADHD). Many studies examined the overlaps and differences across the language deficits in these disorders, but few studies have examined the genetic aspect thereof. In this study, we use a genome-wide approach to evaluate whether common genetic variants increasing risk of SLI may also be associated with ASD and ADHD in the same manner. Our results suggest that this is not the case, and we discuss this finding in the context of theories concerning the etiologies of these disorders. En ligne : http://dx.doi.org/10.1002/aur.2211 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=421 [article] Language deficits in specific language impairment, attention deficit/hyperactivity disorder, and autism spectrum disorder: An analysis of polygenic risk [texte imprimé] / Ron NUDEL, Auteur ; Camilla A.J. CHRISTIANI, Auteur ; Jessica OHLAND, Auteur ; Md Jamal UDDIN, Auteur ; Nicoline HEMAGER, Auteur ; Ditte ELLERSGAARD, Auteur ; Katrine S. SPANG, Auteur ; Birgitte K. BURTON, Auteur ; Aja GREVE, Auteur ; Ditte L. GANTRIIS, Auteur ; Jonas BYBJERG-GRAUHOLM, Auteur ; Jens Richardt MØLLEGAARD JEPSEN, Auteur ; Anne A.E. THORUP, Auteur ; Ole MORS, Auteur ; Merete NORDENTOFT, Auteur ; Thomas WERGE, Auteur . - p.369-381. Langues : Anglais (eng) in Autism Research > 13-3 (March 2020) . - p.369-381 Mots-clés : attention deficit hyperactivity disorder  autism spectrum disorder  genome-wide association study  polygenic risk score  specific language impairment Index. décimale : PER Périodiques Résumé : Language is one of the cognitive domains often impaired across many neurodevelopmental disorders. While for some disorders the linguistic deficit is the primary impairment (e.g., specific language impairment, SLI), for others it may accompany broader behavioral problems (e.g., autism). The precise nature of this phenotypic overlap has been the subject of debate. Moreover, several studies have found genetic overlaps across neurodevelopmental disorders. This raises the question of whether these genetic overlaps may correlate with phenotypic overlaps and, if so, in what manner. Here, we apply a genome-wide approach to the study of the linguistic deficit in SLI, autism spectrum disorder (ASD), and attention deficit/hyperactivity disorder (ADHD). Using a discovery genome-wide association study of SLI, we generate polygenic risk scores (PRS) in an independent sample which includes children with language impairment, SLI, ASD or ADHD and age-matched controls and perform regression analyses across groups. The SLI-trained PRS significantly predicted risk in the SLI case-control group (adjusted R(2) = 6.24%; P = 0.024) but not in the ASD or ADHD case-control groups (adjusted R(2) = 0.0004%, 0.01%; P = 0.984, 0.889, respectively) nor for height, used as a negative control (R(2) = 0.2%; P = 0.452). Additionally, there was a significant difference in the normalized PRS between children with SLI and children with ASD (common language effect size = 0.66; P = 0.044). Our study suggests no additive common-variant genetic overlap between SLI and ASD and ADHD. This is discussed in the context of phenotypic studies of SLI and related disorders. Autism Res 2020, 13: 369-381. (c) 2019 The Authors. Autism Research published by International Society for Autism Research published by Wiley Periodicals, Inc. LAY SUMMARY: Language deficits are characteristic of specific language impairment (SLI), but may also be found in other neurodevelopmental disorders, such as autism spectrum disorder (ASD) and attention deficit/hyperactivity disorder (ADHD). Many studies examined the overlaps and differences across the language deficits in these disorders, but few studies have examined the genetic aspect thereof. In this study, we use a genome-wide approach to evaluate whether common genetic variants increasing risk of SLI may also be associated with ASD and ADHD in the same manner. Our results suggest that this is not the case, and we discuss this finding in the context of theories concerning the etiologies of these disorders. En ligne : http://dx.doi.org/10.1002/aur.2211 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=421

Polygenic risk and hostile environments: Links to stable and dynamic antisocial behaviors across adolescence / Erinn L. ACLAND ; N. POCUCA ; Stéphane PAQUIN ; Michel BOIVIN ; Isabelle OUELLET-MORIN ; T.F.M. ANDLAUER ; J.P. GOUIN ; Sylvana M. CÔTÉ ; Richard E. TREMBLAY ; Marie-Claude GEOFFROY ; Natalie CASTELLANOS-RYAN in Development and Psychopathology, 37-1 (February 2025)  

Public ISBD [article]  inDevelopment and Psychopathology > 37-1 (February 2025) . - p.464-476 Titre : Polygenic risk and hostile environments: Links to stable and dynamic antisocial behaviors across adolescence : Development and Psychopathology Type de document : texte imprimé Auteurs : Erinn L. ACLAND, Auteur ; N. POCUCA, Auteur ; Stéphane PAQUIN, Auteur ; Michel BOIVIN, Auteur ; Isabelle OUELLET-MORIN, Auteur ; T.F.M. ANDLAUER, Auteur ; J.P. GOUIN, Auteur ; Sylvana M. CÔTÉ, Auteur ; Richard E. TREMBLAY, Auteur ; Marie-Claude GEOFFROY, Auteur ; Natalie CASTELLANOS-RYAN, Auteur Article en page(s) : p.464-476 Langues : Anglais (eng) Mots-clés : adolescence  antisocial behavior  environment adversity  longitudinal  polygenic risk score Index. décimale : PER Périodiques Résumé : Adverse environments are linked to elevated youth antisocial behavior. However, this relation is thought to depend, in part, on genetic susceptibility. The present study investigated whether polygenic risk for antisociality moderates relations between hostile environments and stable as well as dynamic antisocial behaviors across adolescence. We derived two antisocial-linked polygenic risk scores (PRS) (N = 721) based on previous genome-wide association studies. Forms of antisocial behavior (nonaggressive conduct problems, physical aggression, social aggression) and environmental hostility (harsh parenting and school violence) were assessed at age 13, 15, and 17 years. Relations to individual differences stable across adolescence (latent stability) vs. time-specific states (timepoint residual variance) of antisocial behavior were assessed via structural equation models. Higher antisocial PRS, harsh parenting, and school violence were linked to stable elevations in antisocial behaviors across adolescence. We identified a consistent polygenic-environment interaction suggestive of differential susceptibility in late adolescence. At age 17, harsher parenting was linked to higher social aggression in those with higher antisocial PRS, and lower social aggression in those with lower antisocial PRS. This suggests that genetics and environmental hostility relate to stable youth antisocial behaviors, and that genetic susceptibility moderates home environment-antisocial associations specifically in late adolescence. En ligne : https://dx.doi.org/10.1017/S095457942400004X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=546 [article] Polygenic risk and hostile environments: Links to stable and dynamic antisocial behaviors across adolescence : Development and Psychopathology [texte imprimé] / Erinn L. ACLAND, Auteur ; N. POCUCA, Auteur ; Stéphane PAQUIN, Auteur ; Michel BOIVIN, Auteur ; Isabelle OUELLET-MORIN, Auteur ; T.F.M. ANDLAUER, Auteur ; J.P. GOUIN, Auteur ; Sylvana M. CÔTÉ, Auteur ; Richard E. TREMBLAY, Auteur ; Marie-Claude GEOFFROY, Auteur ; Natalie CASTELLANOS-RYAN, Auteur . - p.464-476. Langues : Anglais (eng) in Development and Psychopathology > 37-1 (February 2025) . - p.464-476 Mots-clés : adolescence  antisocial behavior  environment adversity  longitudinal  polygenic risk score Index. décimale : PER Périodiques Résumé : Adverse environments are linked to elevated youth antisocial behavior. However, this relation is thought to depend, in part, on genetic susceptibility. The present study investigated whether polygenic risk for antisociality moderates relations between hostile environments and stable as well as dynamic antisocial behaviors across adolescence. We derived two antisocial-linked polygenic risk scores (PRS) (N = 721) based on previous genome-wide association studies. Forms of antisocial behavior (nonaggressive conduct problems, physical aggression, social aggression) and environmental hostility (harsh parenting and school violence) were assessed at age 13, 15, and 17 years. Relations to individual differences stable across adolescence (latent stability) vs. time-specific states (timepoint residual variance) of antisocial behavior were assessed via structural equation models. Higher antisocial PRS, harsh parenting, and school violence were linked to stable elevations in antisocial behaviors across adolescence. We identified a consistent polygenic-environment interaction suggestive of differential susceptibility in late adolescence. At age 17, harsher parenting was linked to higher social aggression in those with higher antisocial PRS, and lower social aggression in those with lower antisocial PRS. This suggests that genetics and environmental hostility relate to stable youth antisocial behaviors, and that genetic susceptibility moderates home environment-antisocial associations specifically in late adolescence. En ligne : https://dx.doi.org/10.1017/S095457942400004X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=546

Prediction of depressive symptoms in young adults by polygenic score and childhood maltreatment: Results from a population-based birth cohort / Marie-Claude GEOFFROY ; Rachel LANGEVIN ; Léa C. PERRET ; Delphine COLLIN-VÉZINA ; Ivan VORONIN ; Jean-Philippe GOUIN ; Xiangfei MENG ; Michel BOIVIN ; Isabelle OUELLET-MORIN in Development and Psychopathology, 37-4 (October 2025)  

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SWAN scale for ADHD trait-based genetic research: a validity and polygenic risk study / Christie L. BURTON in Journal of Child Psychology and Psychiatry, 60-9 (September 2019)  

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Association of polygenic scores for autism with volumetric MRI phenotypes in cerebellum and brainstem in adults / Salahuddin MOHAMMAD in Molecular Autism, 15 (2024)  

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Early manifestations of genetic risk for neurodevelopmental disorders / Ragna Bugge ASKELAND in Journal of Child Psychology and Psychiatry, 63-7 (July 2022)  

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Temperament multi-trajectory groups across adolescence: Associations with adulthood psychopathology and polygenic scores in TRAILS / Frances L. WANG in Development and Psychopathology, 38-2 (May 2026)  

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