6 recherche sur le mot-clé 'polygenic risk scores'

Associations between psychiatric polygenic risk scores and general and specific psychopathology symptoms in childhood and adolescence between and within dizygotic twin pairs / Cen CHEN in Journal of Child Psychology and Psychiatry, 63-12 (December 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-12 (December 2022) . - p.1513-1522 Titre : Associations between psychiatric polygenic risk scores and general and specific psychopathology symptoms in childhood and adolescence between and within dizygotic twin pairs Type de document : Texte imprimé et/ou numérique Auteurs : Cen CHEN, Auteur ; Yi LU, Auteur ; Sebastian LUNDSTROM, Auteur ; Henrik LARSSON, Auteur ; Paul LICHTENSTEIN, Auteur ; Erik PETTERSSON, Auteur Article en page(s) : p.1513-1522 Langues : Anglais (eng) Mots-clés : Adolescent  Humans  Twins, Dizygotic  Longitudinal Studies  Psychopathology  Mental Disorders/epidemiology/genetics  Risk Factors  Attention Deficit Disorder with Hyperactivity/epidemiology  General factor of psychopathology  genetic nurture  multi-polygenic score  polygenic risk scores Index. décimale : PER Périodiques Résumé : BACKGROUND: Although polygenic risk scores (PRS) predict psychiatric problems, these associations might be attributable to indirect pathways including population stratification, assortative mating, or dynastic effects (mediation via parental environments). The goal of this study was to examine whether PRS-psychiatric symptom associations were attributable to indirect versus direct pathways. METHODS: The sample consisted of 3,907 dizygotic (DZ) twin pairs. In childhood, their parents rated them on 98 symptoms. In adolescence (n=2,393 DZ pairs), both the parents and the twins rated themselves on 20 symptoms. We extracted one general and seven specific factors from the childhood data, and one general and three specific factors from the adolescent data. We then regressed each general factor model onto ten psychiatric PRS simultaneously. We first conducted the regressions between individuals (Î2) and then within DZ twin pairs (Î2(w) ), which controls for indirect pathways. RESULTS: In childhood, the PRS for ADHD predicted general psychopathology (Î2=0.09, 95% CI: [0.06, 0.12]; Î2(w) =0.07 [0.01, 0.12]). Furthermore, the PRS for ADHD predicted specific inattention (Î2=0.04 [0.00, 0.08]; Î2(w) =0.09 [0.01, 0.17]) and specific hyperactivity (Î2=0.07 [0.04, 0.11]; Î2(w) =0.09 [0.01, 0.16]); the PRS for schizophrenia predicted specific learning (Î2=0.08 [0.03, 0.13]; Î2(w) =0.19 [0.08, 0.30]) and specific inattention problems (Î2=0.05 [0.01, 0.09]; Î2(w) =0.10 [0.02, 0.19]); and the PRS for neuroticism predicted specific anxiety (Î2=0.06 [0.02, 0.10]; Î2(w) =0.06 [0.00, 0.12]). Overall, the PRS-general factor associations were similar between individuals and within twin pairs, whereas the PRS-specific factors associations amplified by 84% within pairs. CONCLUSIONS: This implies that PRS-psychiatric symptom associations did not appear attributable to indirect pathways such as population stratification, assortative mating, or mediation via parental environments. Rather, genetics appeared to directly influence symptomatology. En ligne : http://dx.doi.org/10.1111/jcpp.13605 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490 [article] Associations between psychiatric polygenic risk scores and general and specific psychopathology symptoms in childhood and adolescence between and within dizygotic twin pairs [Texte imprimé et/ou numérique] / Cen CHEN, Auteur ; Yi LU, Auteur ; Sebastian LUNDSTROM, Auteur ; Henrik LARSSON, Auteur ; Paul LICHTENSTEIN, Auteur ; Erik PETTERSSON, Auteur . - p.1513-1522. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 63-12 (December 2022) . - p.1513-1522 Mots-clés : Adolescent  Humans  Twins, Dizygotic  Longitudinal Studies  Psychopathology  Mental Disorders/epidemiology/genetics  Risk Factors  Attention Deficit Disorder with Hyperactivity/epidemiology  General factor of psychopathology  genetic nurture  multi-polygenic score  polygenic risk scores Index. décimale : PER Périodiques Résumé : BACKGROUND: Although polygenic risk scores (PRS) predict psychiatric problems, these associations might be attributable to indirect pathways including population stratification, assortative mating, or dynastic effects (mediation via parental environments). The goal of this study was to examine whether PRS-psychiatric symptom associations were attributable to indirect versus direct pathways. METHODS: The sample consisted of 3,907 dizygotic (DZ) twin pairs. In childhood, their parents rated them on 98 symptoms. In adolescence (n=2,393 DZ pairs), both the parents and the twins rated themselves on 20 symptoms. We extracted one general and seven specific factors from the childhood data, and one general and three specific factors from the adolescent data. We then regressed each general factor model onto ten psychiatric PRS simultaneously. We first conducted the regressions between individuals (Î2) and then within DZ twin pairs (Î2(w) ), which controls for indirect pathways. RESULTS: In childhood, the PRS for ADHD predicted general psychopathology (Î2=0.09, 95% CI: [0.06, 0.12]; Î2(w) =0.07 [0.01, 0.12]). Furthermore, the PRS for ADHD predicted specific inattention (Î2=0.04 [0.00, 0.08]; Î2(w) =0.09 [0.01, 0.17]) and specific hyperactivity (Î2=0.07 [0.04, 0.11]; Î2(w) =0.09 [0.01, 0.16]); the PRS for schizophrenia predicted specific learning (Î2=0.08 [0.03, 0.13]; Î2(w) =0.19 [0.08, 0.30]) and specific inattention problems (Î2=0.05 [0.01, 0.09]; Î2(w) =0.10 [0.02, 0.19]); and the PRS for neuroticism predicted specific anxiety (Î2=0.06 [0.02, 0.10]; Î2(w) =0.06 [0.00, 0.12]). Overall, the PRS-general factor associations were similar between individuals and within twin pairs, whereas the PRS-specific factors associations amplified by 84% within pairs. CONCLUSIONS: This implies that PRS-psychiatric symptom associations did not appear attributable to indirect pathways such as population stratification, assortative mating, or mediation via parental environments. Rather, genetics appeared to directly influence symptomatology. En ligne : http://dx.doi.org/10.1111/jcpp.13605 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490

Polygenic risk for depression, anxiety and neuroticism are associated with the severity and rate of change in depressive symptoms across adolescence / A. S. F. KWONG in Journal of Child Psychology and Psychiatry, 62-12 (December 2021)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 62-12 (December 2021) . - p.1462-1474 Titre : Polygenic risk for depression, anxiety and neuroticism are associated with the severity and rate of change in depressive symptoms across adolescence Type de document : Texte imprimé et/ou numérique Auteurs : A. S. F. KWONG, Auteur ; T. T. MORRIS, Auteur ; R. M. PEARSON, Auteur ; N. J. TIMPSON, Auteur ; F. RICE, Auteur ; E. STERGIAKOULI, Auteur ; K. TILLING, Auteur Article en page(s) : p.1462-1474 Langues : Anglais (eng) Mots-clés : Adolescent  Adult  Anxiety  Child  Cross-Sectional Studies  Depression/genetics  Depressive Disorder, Major/epidemiology/genetics  Genetic Predisposition to Disease/genetics  Genome-Wide Association Study  Humans  Longitudinal Studies  Multifactorial Inheritance/genetics  Neuroticism  Young Adult  Alspac  Polygenic risk scores  adolescence  depressive symptoms  development  longitudinal  trajectories Index. décimale : PER Périodiques Résumé : BACKGROUND: Adolescence marks a period where depression will commonly onset. Twin studies show that genetic influences play a role in how depression develops and changes across adolescence. Recent genome-wide association studies highlight that common genetic variants - which can be combined into polygenic risk scores (PRS) - are also implicated in depression. However, the role of PRS in adolescent depression and changes in adolescent depression is not yet understood. We aimed to examine associations between PRS for five psychiatric traits and depressive symptoms measured across adolescence using cross-sectional and growth-curve models. The five PRS were as follows: depression (DEP), major depressive disorder (MDD), anxiety (ANX), neuroticism (NEU) and schizophrenia (SCZ). METHODS: We used data from over 6,000 participants of the Avon Longitudinal Study of Parents and Children (ALSPAC) to examine associations between the five PRS and self-reported depressive symptoms (Short Mood and Feelings Questionnaire) over 9 occasions from 10 to 24?years. The PRS were created from well-powered genome-wide association studies conducted in adult populations. We examined cross-sectional associations between the PRS at each age and then again with longitudinal trajectories of depressive symptoms in a repeated measures framework using multilevel growth-curve analysis to examine the severity and the rate of change. RESULTS: There was strong evidence that higher PRS for DEP, MDD and NEU were associated with worse depressive symptoms throughout adolescence and into young adulthood in our cross-sectional analysis, with consistent associations observed across all nine occasions. Growth-curve analyses provided stronger associations (as measured by effect sizes) and additional insights, demonstrating that individuals with higher PRS for DEP, MDD and NEU had steeper trajectories of depressive symptoms across development, all with a greater increasing rate of change during adolescence. Evidence was less consistent for the ANX and SCZ PRS in the cross-sectional analysis, yet there was some evidence for an increasing rate of change in adolescence in the growth-curve analyses with the ANX PRS. CONCLUSIONS: These results show that common genetic variants as indexed by varying psychiatric PRS show patterns of specificity that influence both the severity and rate of change in depressive symptoms throughout adolescence and then into young adulthood. Longitudinal data that make use of repeated measures designs have the potential to provide greater insights how genetic factors influence the onset and persistence of adolescent depression. En ligne : http://dx.doi.org/10.1111/jcpp.13422 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456 [article] Polygenic risk for depression, anxiety and neuroticism are associated with the severity and rate of change in depressive symptoms across adolescence [Texte imprimé et/ou numérique] / A. S. F. KWONG, Auteur ; T. T. MORRIS, Auteur ; R. M. PEARSON, Auteur ; N. J. TIMPSON, Auteur ; F. RICE, Auteur ; E. STERGIAKOULI, Auteur ; K. TILLING, Auteur . - p.1462-1474. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 62-12 (December 2021) . - p.1462-1474 Mots-clés : Adolescent  Adult  Anxiety  Child  Cross-Sectional Studies  Depression/genetics  Depressive Disorder, Major/epidemiology/genetics  Genetic Predisposition to Disease/genetics  Genome-Wide Association Study  Humans  Longitudinal Studies  Multifactorial Inheritance/genetics  Neuroticism  Young Adult  Alspac  Polygenic risk scores  adolescence  depressive symptoms  development  longitudinal  trajectories Index. décimale : PER Périodiques Résumé : BACKGROUND: Adolescence marks a period where depression will commonly onset. Twin studies show that genetic influences play a role in how depression develops and changes across adolescence. Recent genome-wide association studies highlight that common genetic variants - which can be combined into polygenic risk scores (PRS) - are also implicated in depression. However, the role of PRS in adolescent depression and changes in adolescent depression is not yet understood. We aimed to examine associations between PRS for five psychiatric traits and depressive symptoms measured across adolescence using cross-sectional and growth-curve models. The five PRS were as follows: depression (DEP), major depressive disorder (MDD), anxiety (ANX), neuroticism (NEU) and schizophrenia (SCZ). METHODS: We used data from over 6,000 participants of the Avon Longitudinal Study of Parents and Children (ALSPAC) to examine associations between the five PRS and self-reported depressive symptoms (Short Mood and Feelings Questionnaire) over 9 occasions from 10 to 24?years. The PRS were created from well-powered genome-wide association studies conducted in adult populations. We examined cross-sectional associations between the PRS at each age and then again with longitudinal trajectories of depressive symptoms in a repeated measures framework using multilevel growth-curve analysis to examine the severity and the rate of change. RESULTS: There was strong evidence that higher PRS for DEP, MDD and NEU were associated with worse depressive symptoms throughout adolescence and into young adulthood in our cross-sectional analysis, with consistent associations observed across all nine occasions. Growth-curve analyses provided stronger associations (as measured by effect sizes) and additional insights, demonstrating that individuals with higher PRS for DEP, MDD and NEU had steeper trajectories of depressive symptoms across development, all with a greater increasing rate of change during adolescence. Evidence was less consistent for the ANX and SCZ PRS in the cross-sectional analysis, yet there was some evidence for an increasing rate of change in adolescence in the growth-curve analyses with the ANX PRS. CONCLUSIONS: These results show that common genetic variants as indexed by varying psychiatric PRS show patterns of specificity that influence both the severity and rate of change in depressive symptoms throughout adolescence and then into young adulthood. Longitudinal data that make use of repeated measures designs have the potential to provide greater insights how genetic factors influence the onset and persistence of adolescent depression. En ligne : http://dx.doi.org/10.1111/jcpp.13422 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456

The effects of life experiences and polygenic risk for depression on the development of positive and negative cognitive biases across adolescence: The CogBIAS hypothesis / Orestis Zavlis ; Sam PARSONS ; Elaine FOX ; Charlotte BOOTH ; Annabel SONGCO ; John Paul Vincent in Development and Psychopathology, 37-1 (February 2025)  

Public ISBD [article]  inDevelopment and Psychopathology > 37-1 (February 2025) . - p.361-370 Titre : The effects of life experiences and polygenic risk for depression on the development of positive and negative cognitive biases across adolescence: The CogBIAS hypothesis : Development and Psychopathology Type de document : Texte imprimé et/ou numérique Auteurs : Orestis Zavlis, Auteur ; Sam PARSONS, Auteur ; Elaine FOX, Auteur ; Charlotte BOOTH, Auteur ; Annabel SONGCO, Auteur ; John Paul Vincent, Auteur Article en page(s) : p.361-370 Langues : Anglais (eng) Mots-clés : Adolescence  cognitive biases  life experiences  polygenic risk scores  psychopathology Index. décimale : PER Périodiques Résumé : The Cognitive Bias (CogBIAS) hypothesis proposes that cognitive biases develop as a function of environmental influences (which determine the valence of biases) and the genetic susceptibility to those influences (which determines the potency of biases). The current study employed a longitudinal, polygenic-by-environment approach to examine the CogBIAS hypothesis. To this end, measures of life experiences and polygenic scores for depression were used to assess the development of memory and interpretation biases in a three-wave sample of adolescents (12-16 years) (N = 337). Using mixed effects modeling, three patterns were revealed. First, positive life experiences (PLEs) were found to diminish negative and enhance positive forms of memory and social interpretation biases. Second, and against expectation, negative life experiences and depression polygenic scores were not associated with any cognitive outcomes, upon adjusting for psychopathology. Finally, and most importantly, the interaction between high polygenic risk and greater PLEs was associated with a stronger positive interpretation bias for social situations. These results provide the first line of polygenic evidence in support of the CogBIAS hypothesis, but also extend this hypothesis by highlighting positive genetic and nuanced environmental influences on the development of cognitive biases across adolescence. En ligne : https://dx.doi.org/10.1017/S0954579423001645 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=546 [article] The effects of life experiences and polygenic risk for depression on the development of positive and negative cognitive biases across adolescence: The CogBIAS hypothesis : Development and Psychopathology [Texte imprimé et/ou numérique] / Orestis Zavlis, Auteur ; Sam PARSONS, Auteur ; Elaine FOX, Auteur ; Charlotte BOOTH, Auteur ; Annabel SONGCO, Auteur ; John Paul Vincent, Auteur . - p.361-370. Langues : Anglais (eng) in Development and Psychopathology > 37-1 (February 2025) . - p.361-370 Mots-clés : Adolescence  cognitive biases  life experiences  polygenic risk scores  psychopathology Index. décimale : PER Périodiques Résumé : The Cognitive Bias (CogBIAS) hypothesis proposes that cognitive biases develop as a function of environmental influences (which determine the valence of biases) and the genetic susceptibility to those influences (which determines the potency of biases). The current study employed a longitudinal, polygenic-by-environment approach to examine the CogBIAS hypothesis. To this end, measures of life experiences and polygenic scores for depression were used to assess the development of memory and interpretation biases in a three-wave sample of adolescents (12-16 years) (N = 337). Using mixed effects modeling, three patterns were revealed. First, positive life experiences (PLEs) were found to diminish negative and enhance positive forms of memory and social interpretation biases. Second, and against expectation, negative life experiences and depression polygenic scores were not associated with any cognitive outcomes, upon adjusting for psychopathology. Finally, and most importantly, the interaction between high polygenic risk and greater PLEs was associated with a stronger positive interpretation bias for social situations. These results provide the first line of polygenic evidence in support of the CogBIAS hypothesis, but also extend this hypothesis by highlighting positive genetic and nuanced environmental influences on the development of cognitive biases across adolescence. En ligne : https://dx.doi.org/10.1017/S0954579423001645 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=546

Genetic susceptibility for major depressive disorder associates with trajectories of depressive symptoms across childhood and adolescence / A. A. LUSSIER in Journal of Child Psychology and Psychiatry, 62-7 (July 2021)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 62-7 (July 2021) . - p.895-904 Titre : Genetic susceptibility for major depressive disorder associates with trajectories of depressive symptoms across childhood and adolescence Type de document : Texte imprimé et/ou numérique Auteurs : A. A. LUSSIER, Auteur ; M. HAWRILENKO, Auteur ; M. J. WANG, Auteur ; Karmel W. CHOI, Auteur ; J. CERUTTI, Auteur ; Y. ZHU, Auteur ; E. C. DUNN, Auteur Article en page(s) : p.895-904 Langues : Anglais (eng) Mots-clés : Adolescent  Adult  Child  Depression  Depressive Disorder, Major/epidemiology/genetics  Genetic Predisposition to Disease/genetics  Genome-Wide Association Study  Humans  Longitudinal Studies  Prospective Studies  Alspac  Depression trajectories  development  longitudinal  polygenic risk scores Index. décimale : PER Périodiques Résumé : BACKGROUND: Early-onset depression during childhood and adolescence is associated with a worse course of illness and outcome than adult onset. However, the genetic factors that influence risk for early-onset depression remain mostly unknown. Using data collected over 13 years, we examined whether polygenic risk scores (PRS) that capture genetic risk for depression were associated with depressive symptom trajectories assessed from childhood to adolescence. METHODS: Data came from the Avon Longitudinal Study of Parents and Children, a prospective, longitudinal birth cohort (analytic sample = 7,308 youth). We analyzed the relationship between genetic susceptibility to depression and three time-dependent measures of depressive symptoms trajectories spanning 4-16.5 years of age (class, onset, and cumulative burden). Trajectories were constructed using a growth mixture model with structured residuals. PRS were generated from the summary statistics of a genome-wide association study of depression risk using data from the Psychiatric Genomics Consortium, UK Biobank, and 23andMe, Inc. We used MAGMA to identify gene-level associations with these measures. RESULTS: Youth were classified into six classes of depressive symptom trajectories: high/renitent (27.9% of youth), high/reversing (9.1%), childhood decrease (7.3%), late childhood peak (3.3%), adolescent spike (2.5%), and minimal symptoms (49.9%). PRS discriminated between youth in the late childhood peak, high/reversing, and high/renitent classes compared to the minimal symptoms and childhood decrease classes. No significant associations were detected at the gene level. CONCLUSIONS: This study highlights differences in polygenic loading for depressive symptoms across childhood and adolescence, particularly among youths with high symptoms in early adolescence, regardless of age-independent patterns. En ligne : http://dx.doi.org/10.1111/jcpp.13342 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456 [article] Genetic susceptibility for major depressive disorder associates with trajectories of depressive symptoms across childhood and adolescence [Texte imprimé et/ou numérique] / A. A. LUSSIER, Auteur ; M. HAWRILENKO, Auteur ; M. J. WANG, Auteur ; Karmel W. CHOI, Auteur ; J. CERUTTI, Auteur ; Y. ZHU, Auteur ; E. C. DUNN, Auteur . - p.895-904. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 62-7 (July 2021) . - p.895-904 Mots-clés : Adolescent  Adult  Child  Depression  Depressive Disorder, Major/epidemiology/genetics  Genetic Predisposition to Disease/genetics  Genome-Wide Association Study  Humans  Longitudinal Studies  Prospective Studies  Alspac  Depression trajectories  development  longitudinal  polygenic risk scores Index. décimale : PER Périodiques Résumé : BACKGROUND: Early-onset depression during childhood and adolescence is associated with a worse course of illness and outcome than adult onset. However, the genetic factors that influence risk for early-onset depression remain mostly unknown. Using data collected over 13 years, we examined whether polygenic risk scores (PRS) that capture genetic risk for depression were associated with depressive symptom trajectories assessed from childhood to adolescence. METHODS: Data came from the Avon Longitudinal Study of Parents and Children, a prospective, longitudinal birth cohort (analytic sample = 7,308 youth). We analyzed the relationship between genetic susceptibility to depression and three time-dependent measures of depressive symptoms trajectories spanning 4-16.5 years of age (class, onset, and cumulative burden). Trajectories were constructed using a growth mixture model with structured residuals. PRS were generated from the summary statistics of a genome-wide association study of depression risk using data from the Psychiatric Genomics Consortium, UK Biobank, and 23andMe, Inc. We used MAGMA to identify gene-level associations with these measures. RESULTS: Youth were classified into six classes of depressive symptom trajectories: high/renitent (27.9% of youth), high/reversing (9.1%), childhood decrease (7.3%), late childhood peak (3.3%), adolescent spike (2.5%), and minimal symptoms (49.9%). PRS discriminated between youth in the late childhood peak, high/reversing, and high/renitent classes compared to the minimal symptoms and childhood decrease classes. No significant associations were detected at the gene level. CONCLUSIONS: This study highlights differences in polygenic loading for depressive symptoms across childhood and adolescence, particularly among youths with high symptoms in early adolescence, regardless of age-independent patterns. En ligne : http://dx.doi.org/10.1111/jcpp.13342 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456

Pupil size and pupillary light reflex in early infancy: heritability and link to genetic liability to schizophrenia / Ana Maria PORTUGAL in Journal of Child Psychology and Psychiatry, 63-9 (September 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-9 (September 2022) . - p.1068-1077 Titre : Pupil size and pupillary light reflex in early infancy: heritability and link to genetic liability to schizophrenia Type de document : Texte imprimé et/ou numérique Auteurs : Ana Maria PORTUGAL, Auteur ; Mark J. TAYLOR, Auteur ; Charlotte VIKTORSSON, Auteur ; Pär NYSTROM, Auteur ; Danyang LI, Auteur ; Kristiina TAMMIMIES, Auteur ; Angelica RONALD, Auteur ; Terje FALCK-YTTER, Auteur Article en page(s) : p.1068-1077 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder  Depressive Disorder, Major  Humans  Infant  Pupil/physiology  Reflex, Pupillary/physiology  Schizophrenia/genetics  Pupillometry  infancy  polygenic risk scores  pupillary light reflex  schizophrenia  twin design Index. décimale : PER Périodiques Résumé : BACKGROUND: Measures based on pupillometry, such as the pupillary light reflex (PLR) and baseline pupil size, reflect physiological responses linked to specific neural circuits that have been implicated as atypical in some psychiatric and neurodevelopmental conditions. METHODS: We investigated the contribution of genetic and environmental factors to the baseline pupil size and the PLR in 510 infant twins assessed at 5months of age (281 monozygotic and 229 dizygotic pairs), and its associations with common genetic variants associated with neurodevelopmental (autism spectrum disorder and attention deficit hyperactivity disorder) and mental health (bipolar disorder, major depressive disorder and schizophrenia) conditions using genome-wide polygenic scores (GPSs). RESULTS: Univariate twin modelling showed high heritability at 5months for both pupil size (h(2) =.64) and constriction in response to light (h(2) =.62), and bivariate twin modeling indicated substantial independence between the genetic factors influencing each (r(G) =.38). A statistically significant positive association between infant tonic pupil size and the GPS for schizophrenia was found (Î2=.15, p=.024), while there was no significant association with the GPS for autism or any other GPSs. CONCLUSIONS: This study shows that some pupil measures are highly heritable in early infancy, although substantially independent in their genetic etiologies, and associated with common genetic variants linked to schizophrenia. It illustrates how genetically informed studies of infants may help us understand early physiological responses associated with psychiatric disorders which emerge much later in life. En ligne : http://dx.doi.org/10.1111/jcpp.13564 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486 [article] Pupil size and pupillary light reflex in early infancy: heritability and link to genetic liability to schizophrenia [Texte imprimé et/ou numérique] / Ana Maria PORTUGAL, Auteur ; Mark J. TAYLOR, Auteur ; Charlotte VIKTORSSON, Auteur ; Pär NYSTROM, Auteur ; Danyang LI, Auteur ; Kristiina TAMMIMIES, Auteur ; Angelica RONALD, Auteur ; Terje FALCK-YTTER, Auteur . - p.1068-1077. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 63-9 (September 2022) . - p.1068-1077 Mots-clés : Autism Spectrum Disorder  Depressive Disorder, Major  Humans  Infant  Pupil/physiology  Reflex, Pupillary/physiology  Schizophrenia/genetics  Pupillometry  infancy  polygenic risk scores  pupillary light reflex  schizophrenia  twin design Index. décimale : PER Périodiques Résumé : BACKGROUND: Measures based on pupillometry, such as the pupillary light reflex (PLR) and baseline pupil size, reflect physiological responses linked to specific neural circuits that have been implicated as atypical in some psychiatric and neurodevelopmental conditions. METHODS: We investigated the contribution of genetic and environmental factors to the baseline pupil size and the PLR in 510 infant twins assessed at 5months of age (281 monozygotic and 229 dizygotic pairs), and its associations with common genetic variants associated with neurodevelopmental (autism spectrum disorder and attention deficit hyperactivity disorder) and mental health (bipolar disorder, major depressive disorder and schizophrenia) conditions using genome-wide polygenic scores (GPSs). RESULTS: Univariate twin modelling showed high heritability at 5months for both pupil size (h(2) =.64) and constriction in response to light (h(2) =.62), and bivariate twin modeling indicated substantial independence between the genetic factors influencing each (r(G) =.38). A statistically significant positive association between infant tonic pupil size and the GPS for schizophrenia was found (Î2=.15, p=.024), while there was no significant association with the GPS for autism or any other GPSs. CONCLUSIONS: This study shows that some pupil measures are highly heritable in early infancy, although substantially independent in their genetic etiologies, and associated with common genetic variants linked to schizophrenia. It illustrates how genetically informed studies of infants may help us understand early physiological responses associated with psychiatric disorders which emerge much later in life. En ligne : http://dx.doi.org/10.1111/jcpp.13564 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486

Heterotypic trajectories of dimensional psychopathology across the lifespan: the case of youth-onset attention deficit/hyperactivity disorder / A. G. MANFRO in Journal of Child Psychology and Psychiatry, 60-5 (May 2019)  

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