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Auteur Andrea G. ALLEGRINI |
Documents disponibles écrits par cet auteur (7)



Editorial: Does the polygenic revolution herald a watershed in the study of GE interplay in developmental psychopathology? Some considerations for the Special Issue reader / Edward D. BARKER in Journal of Child Psychology and Psychiatry, 63-10 (October 2022)
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[article]
Titre : Editorial: Does the polygenic revolution herald a watershed in the study of GE interplay in developmental psychopathology? Some considerations for the Special Issue reader Type de document : Texte imprimé et/ou numérique Auteurs : Edward D. BARKER, Auteur ; Barbara MAUGHAN, Auteur ; Andrea G. ALLEGRINI, Auteur ; Jean Baptiste PINGAULT, Auteur ; Edmund J. S. SONUGA-BARKE, Auteur Année de publication : 2022 Article en page(s) : p.1107-1110 Langues : Anglais (eng) Mots-clés : Child Humans Mental Disorders/genetics/psychology Psychopathology Receptor for Advanced Glycation End Products Risk Factors Index. décimale : PER Périodiques Résumé : The primary goal motivating the scientific field of Developmental Psychopathology is to discover why some individuals develop mental health and neuro-developmental difficulties while others do not. This is not simply a 'blue skies' preoccupation: the underlying hope, of course, is to translate such discoveries to the benefit of individuals, families and communities, reducing poor outcomes for those at risk and - in the best case scenario - ensuring that they thrive. A core tenet of the bio-psycho-social framework within which this field of enquiry operates is that children's difficulties are determined by the interplay of predisposing genetic risk and resilience factors and the environments and experiences to which individuals are exposed. From this perspective, understanding gene-environment (GE) interplay is a necessary condition for explaining and, as importantly predicting, why one individual is at risk while another is not. If we believe this, then the risk calculators designed to show who will and will not get a particular disorder - all the rage at the moment - are doomed to fail until they can go beyond modelling the main effects of genes and environments, and reliably estimate GE processes too. Despite significant progress, we remain a considerable way off cracking this problem. En ligne : http://dx.doi.org/10.1111/jcpp.13692 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486
in Journal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1107-1110[article] Editorial: Does the polygenic revolution herald a watershed in the study of GE interplay in developmental psychopathology? Some considerations for the Special Issue reader [Texte imprimé et/ou numérique] / Edward D. BARKER, Auteur ; Barbara MAUGHAN, Auteur ; Andrea G. ALLEGRINI, Auteur ; Jean Baptiste PINGAULT, Auteur ; Edmund J. S. SONUGA-BARKE, Auteur . - 2022 . - p.1107-1110.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1107-1110
Mots-clés : Child Humans Mental Disorders/genetics/psychology Psychopathology Receptor for Advanced Glycation End Products Risk Factors Index. décimale : PER Périodiques Résumé : The primary goal motivating the scientific field of Developmental Psychopathology is to discover why some individuals develop mental health and neuro-developmental difficulties while others do not. This is not simply a 'blue skies' preoccupation: the underlying hope, of course, is to translate such discoveries to the benefit of individuals, families and communities, reducing poor outcomes for those at risk and - in the best case scenario - ensuring that they thrive. A core tenet of the bio-psycho-social framework within which this field of enquiry operates is that children's difficulties are determined by the interplay of predisposing genetic risk and resilience factors and the environments and experiences to which individuals are exposed. From this perspective, understanding gene-environment (GE) interplay is a necessary condition for explaining and, as importantly predicting, why one individual is at risk while another is not. If we believe this, then the risk calculators designed to show who will and will not get a particular disorder - all the rage at the moment - are doomed to fail until they can go beyond modelling the main effects of genes and environments, and reliably estimate GE processes too. Despite significant progress, we remain a considerable way off cracking this problem. En ligne : http://dx.doi.org/10.1111/jcpp.13692 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486 Gene × Environment contributions to autonomic stress reactivity in youth / Andrea G. ALLEGRINI in Development and Psychopathology, 31-1 (February 2019)
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Titre : Gene × Environment contributions to autonomic stress reactivity in youth Type de document : Texte imprimé et/ou numérique Auteurs : Andrea G. ALLEGRINI, Auteur ; Brittany E. EVANS, Auteur ; Susanne DE ROOIJ, Auteur ; Kirstin GREAVES-LORD, Auteur ; Anja C. HUIZINK, Auteur Article en page(s) : p.293-307 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Dysregulated physiological stress reactivity has been suggested to impact the development of children and adolescents with important health consequences throughout the life span. Both environmental adversity and genetic predispositions can lead to physiological imbalances in stress systems, which in turn lead to developmental differences. We investigated genetic and environmental contributions to autonomic nervous system reactivity to a psychosocial stressor. Furthermore, we tested whether these effects were consistent with the differential susceptibility framework. Composite measures of adverse life events combined with socioeconomic status were constructed. Effects of these adversity scores in interaction with a polygenic score summarizing six genetic variants, which were hypothesized to work as susceptibility factors, were tested on autonomic nervous system measures as indexed by heart rate and heart rate variability. Results showed that carriers of more genetic variants and exposed to high adversity manifested enhanced heart rate variability reactivity to a psychosocial stressor compared to carriers of fewer genetic variants. Conversely, the stress procedure elicited a more moderate response in these individuals compared to carriers of fewer variants when adversity was low. En ligne : http://dx.doi.org/10.1017/S095457941700181X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=383
in Development and Psychopathology > 31-1 (February 2019) . - p.293-307[article] Gene × Environment contributions to autonomic stress reactivity in youth [Texte imprimé et/ou numérique] / Andrea G. ALLEGRINI, Auteur ; Brittany E. EVANS, Auteur ; Susanne DE ROOIJ, Auteur ; Kirstin GREAVES-LORD, Auteur ; Anja C. HUIZINK, Auteur . - p.293-307.
Langues : Anglais (eng)
in Development and Psychopathology > 31-1 (February 2019) . - p.293-307
Index. décimale : PER Périodiques Résumé : Dysregulated physiological stress reactivity has been suggested to impact the development of children and adolescents with important health consequences throughout the life span. Both environmental adversity and genetic predispositions can lead to physiological imbalances in stress systems, which in turn lead to developmental differences. We investigated genetic and environmental contributions to autonomic nervous system reactivity to a psychosocial stressor. Furthermore, we tested whether these effects were consistent with the differential susceptibility framework. Composite measures of adverse life events combined with socioeconomic status were constructed. Effects of these adversity scores in interaction with a polygenic score summarizing six genetic variants, which were hypothesized to work as susceptibility factors, were tested on autonomic nervous system measures as indexed by heart rate and heart rate variability. Results showed that carriers of more genetic variants and exposed to high adversity manifested enhanced heart rate variability reactivity to a psychosocial stressor compared to carriers of fewer genetic variants. Conversely, the stress procedure elicited a more moderate response in these individuals compared to carriers of fewer variants when adversity was low. En ligne : http://dx.doi.org/10.1017/S095457941700181X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=383 Genetic and phenotypic heterogeneity in early neurodevelopmental traits in the Norwegian Mother, Father and Child Cohort Study / Laura HEGEMANN in Molecular Autism, 15 (2024)
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Titre : Genetic and phenotypic heterogeneity in early neurodevelopmental traits in the Norwegian Mother, Father and Child Cohort Study Type de document : Texte imprimé et/ou numérique Auteurs : Laura HEGEMANN, Auteur ; Elizabeth C. CORFIELD, Auteur ; Adrian Dahl ASKELUND, Auteur ; Andrea G. ALLEGRINI, Auteur ; Ragna Bugge ASKELAND, Auteur ; Angelica RONALD, Auteur ; Helga ASK, Auteur ; Beate ST POURCAIN, Auteur ; Ole A. ANDREASSEN, Auteur ; Laurie J. HANNIGAN, Auteur ; Alexandra. HAVDAHL, Auteur Article en page(s) : 25p. Langues : Anglais (eng) Mots-clés : Humans Norway Female Male Phenotype Child, Preschool Cohort Studies Neurodevelopmental Disorders/genetics/diagnosis Mothers Autistic Disorder/genetics Genetic Predisposition to Disease Adult Fathers Genome-Wide Association Study Attention Deficit Disorder with Hyperactivity/genetics/diagnosis Schizophrenia/genetics Genetic Heterogeneity Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism and different neurodevelopmental conditions frequently co-occur, as do their symptoms at sub-diagnostic threshold levels. Overlapping traits and shared genetic liability are potential explanations. METHODS: In the population-based Norwegian Mother, Father, and Child Cohort study (MoBa), we leverage item-level data to explore the phenotypic factor structure and genetic architecture underlying neurodevelopmental traits at age 3 years (N = 41,708-58,630) using maternal reports on 76 items assessing children's motor and language development, social functioning, communication, attention, activity regulation, and flexibility of behaviors and interests. RESULTS: We identified 11 latent factors at the phenotypic level. These factors showed associations with diagnoses of autism and other neurodevelopmental conditions. Most shared genetic liabilities with autism, ADHD, and/or schizophrenia. Item-level GWAS revealed trait-specific genetic correlations with autism (items r(g) range = -?0.27-0.78), ADHD (items r(g) range = -?0.40-1), and schizophrenia (items r(g) range = -?0.24-0.34). We find little evidence of common genetic liability across all neurodevelopmental traits but more so for several genetic factors across more specific areas of neurodevelopment, particularly social and communication traits. Some of these factors, such as one capturing prosocial behavior, overlap with factors found in the phenotypic analyses. Other areas, such as motor development, seemed to have more heterogenous etiology, with specific traits showing a less consistent pattern of genetic correlations with each other. CONCLUSIONS: These exploratory findings emphasize the etiological complexity of neurodevelopmental traits at this early age. In particular, diverse associations with neurodevelopmental conditions and genetic heterogeneity could inform follow-up work to identify shared and differentiating factors in the early manifestations of neurodevelopmental traits and their relation to autism and other neurodevelopmental conditions. This in turn could have implications for clinical screening tools and programs. En ligne : https://dx.doi.org/10.1186/s13229-024-00599-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538
in Molecular Autism > 15 (2024) . - 25p.[article] Genetic and phenotypic heterogeneity in early neurodevelopmental traits in the Norwegian Mother, Father and Child Cohort Study [Texte imprimé et/ou numérique] / Laura HEGEMANN, Auteur ; Elizabeth C. CORFIELD, Auteur ; Adrian Dahl ASKELUND, Auteur ; Andrea G. ALLEGRINI, Auteur ; Ragna Bugge ASKELAND, Auteur ; Angelica RONALD, Auteur ; Helga ASK, Auteur ; Beate ST POURCAIN, Auteur ; Ole A. ANDREASSEN, Auteur ; Laurie J. HANNIGAN, Auteur ; Alexandra. HAVDAHL, Auteur . - 25p.
Langues : Anglais (eng)
in Molecular Autism > 15 (2024) . - 25p.
Mots-clés : Humans Norway Female Male Phenotype Child, Preschool Cohort Studies Neurodevelopmental Disorders/genetics/diagnosis Mothers Autistic Disorder/genetics Genetic Predisposition to Disease Adult Fathers Genome-Wide Association Study Attention Deficit Disorder with Hyperactivity/genetics/diagnosis Schizophrenia/genetics Genetic Heterogeneity Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism and different neurodevelopmental conditions frequently co-occur, as do their symptoms at sub-diagnostic threshold levels. Overlapping traits and shared genetic liability are potential explanations. METHODS: In the population-based Norwegian Mother, Father, and Child Cohort study (MoBa), we leverage item-level data to explore the phenotypic factor structure and genetic architecture underlying neurodevelopmental traits at age 3 years (N = 41,708-58,630) using maternal reports on 76 items assessing children's motor and language development, social functioning, communication, attention, activity regulation, and flexibility of behaviors and interests. RESULTS: We identified 11 latent factors at the phenotypic level. These factors showed associations with diagnoses of autism and other neurodevelopmental conditions. Most shared genetic liabilities with autism, ADHD, and/or schizophrenia. Item-level GWAS revealed trait-specific genetic correlations with autism (items r(g) range = -?0.27-0.78), ADHD (items r(g) range = -?0.40-1), and schizophrenia (items r(g) range = -?0.24-0.34). We find little evidence of common genetic liability across all neurodevelopmental traits but more so for several genetic factors across more specific areas of neurodevelopment, particularly social and communication traits. Some of these factors, such as one capturing prosocial behavior, overlap with factors found in the phenotypic analyses. Other areas, such as motor development, seemed to have more heterogenous etiology, with specific traits showing a less consistent pattern of genetic correlations with each other. CONCLUSIONS: These exploratory findings emphasize the etiological complexity of neurodevelopmental traits at this early age. In particular, diverse associations with neurodevelopmental conditions and genetic heterogeneity could inform follow-up work to identify shared and differentiating factors in the early manifestations of neurodevelopmental traits and their relation to autism and other neurodevelopmental conditions. This in turn could have implications for clinical screening tools and programs. En ligne : https://dx.doi.org/10.1186/s13229-024-00599-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538 Research Review: A guide to computing and implementing polygenic scores in developmental research / Andrea G. ALLEGRINI in Journal of Child Psychology and Psychiatry, 63-10 (October 2022)
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Titre : Research Review: A guide to computing and implementing polygenic scores in developmental research Type de document : Texte imprimé et/ou numérique Auteurs : Andrea G. ALLEGRINI, Auteur ; Jessie R. BALDWIN, Auteur ; Wikus BARKHUIZEN, Auteur ; Jean-Baptiste PINGAULT, Auteur Année de publication : 2022 Article en page(s) : p.1111-1124 Langues : Anglais (eng) Mots-clés : Adolescent Child Genotype Humans Multifactorial Inheritance/genetics Polygenic scores developmental research longitudinal models Index. décimale : PER Périodiques Résumé : The increasing availability of genotype data in longitudinal population- and family-based samples provides opportunities for using polygenic scores (PGS) to study developmental questions in child and adolescent psychology and psychiatry. Here, we aim to provide a comprehensive overview of how PGS can be generated and implemented in developmental psycho(patho)logy, with a focus on longitudinal designs. As such, the paper is organized into three parts: First, we provide a formal definition of polygenic scores and related concepts, focusing on assumptions and limitations. Second, we give a general overview of the methods used to compute polygenic scores, ranging from the classic approach to more advanced methods. We include recommendations and reference resources available to researchers aiming to conduct PGS analyses. Finally, we focus on the practical applications of PGS in the analysis of longitudinal data. We describe how PGS have been used to research developmental outcomes, and how they can be applied to longitudinal data to address developmental questions. En ligne : http://dx.doi.org/10.1111/jcpp.13611 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486
in Journal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1111-1124[article] Research Review: A guide to computing and implementing polygenic scores in developmental research [Texte imprimé et/ou numérique] / Andrea G. ALLEGRINI, Auteur ; Jessie R. BALDWIN, Auteur ; Wikus BARKHUIZEN, Auteur ; Jean-Baptiste PINGAULT, Auteur . - 2022 . - p.1111-1124.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1111-1124
Mots-clés : Adolescent Child Genotype Humans Multifactorial Inheritance/genetics Polygenic scores developmental research longitudinal models Index. décimale : PER Périodiques Résumé : The increasing availability of genotype data in longitudinal population- and family-based samples provides opportunities for using polygenic scores (PGS) to study developmental questions in child and adolescent psychology and psychiatry. Here, we aim to provide a comprehensive overview of how PGS can be generated and implemented in developmental psycho(patho)logy, with a focus on longitudinal designs. As such, the paper is organized into three parts: First, we provide a formal definition of polygenic scores and related concepts, focusing on assumptions and limitations. Second, we give a general overview of the methods used to compute polygenic scores, ranging from the classic approach to more advanced methods. We include recommendations and reference resources available to researchers aiming to conduct PGS analyses. Finally, we focus on the practical applications of PGS in the analysis of longitudinal data. We describe how PGS have been used to research developmental outcomes, and how they can be applied to longitudinal data to address developmental questions. En ligne : http://dx.doi.org/10.1111/jcpp.13611 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486 Research Review: How to interpret associations between polygenic scores, environmental risks, and phenotypes / Jean-Baptiste PINGAULT in Journal of Child Psychology and Psychiatry, 63-10 (October 2022)
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Titre : Research Review: How to interpret associations between polygenic scores, environmental risks, and phenotypes Type de document : Texte imprimé et/ou numérique Auteurs : Jean-Baptiste PINGAULT, Auteur ; Andrea G. ALLEGRINI, Auteur ; Tracy ODIGIE, Auteur ; Leonard FRACH, Auteur ; Jessie R. BALDWIN, Auteur ; Frühling V. RIJSDIJK, Auteur ; Frank DUDBRIDGE, Auteur Année de publication : 2022 Article en page(s) : p.1125-1139 Langues : Anglais (eng) Mots-clés : Cohort Studies Environmental Exposure/adverse effects Genetic Predisposition to Disease Genome-Wide Association Study Humans Midazolam Multifactorial Inheritance Phenotype Polygenic scores biases environment epidemiology phenotypes Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic influences are ubiquitous as virtually all phenotypes and most exposures typically classified as environmental have been found to be heritable. A polygenic score summarises the associations between millions of genetic variants and an outcome in a single value for each individual. Ever lowering costs have enabled the genotyping of many samples relevant to child psychology and psychiatry research, including cohort studies, leading to the proliferation of polygenic score studies. It is tempting to assume that associations detected between polygenic scores and phenotypes in those studies only reflect genetic effects. However, such associations can reflect many pathways (e.g. via environmental mediation) and biases. METHODS: Here, we provide a comprehensive overview of the many reasons why associations between polygenic scores, environmental exposures, and phenotypes exist. We include formal representations of common analyses in polygenic score studies using structural equation modelling. We derive biases, provide illustrative empirical examples and, when possible, mention steps that can be taken to alleviate those biases. RESULTS: Structural equation models and derivations show the many complexities arising from jointly modelling polygenic scores with environmental exposures and phenotypes. Counter-intuitive examples include that: (a) associations between polygenic scores and phenotypes may exist even in the absence of direct genetic effects; (b) associations between child polygenic scores and environmental exposures can exist in the absence of evocative/active gene-environment correlations; and (c) adjusting an exposure-outcome association for a polygenic score can increase rather than decrease bias. CONCLUSIONS: Strikingly, using polygenic scores may, in some cases, lead to more bias than not using them. Appropriately conducting and interpreting polygenic score studies thus requires researchers in child psychology and psychiatry and beyond to be versed in both epidemiological and genetic methods or build on interdisciplinary collaborations. En ligne : http://dx.doi.org/10.1111/jcpp.13607 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486
in Journal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1125-1139[article] Research Review: How to interpret associations between polygenic scores, environmental risks, and phenotypes [Texte imprimé et/ou numérique] / Jean-Baptiste PINGAULT, Auteur ; Andrea G. ALLEGRINI, Auteur ; Tracy ODIGIE, Auteur ; Leonard FRACH, Auteur ; Jessie R. BALDWIN, Auteur ; Frühling V. RIJSDIJK, Auteur ; Frank DUDBRIDGE, Auteur . - 2022 . - p.1125-1139.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1125-1139
Mots-clés : Cohort Studies Environmental Exposure/adverse effects Genetic Predisposition to Disease Genome-Wide Association Study Humans Midazolam Multifactorial Inheritance Phenotype Polygenic scores biases environment epidemiology phenotypes Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic influences are ubiquitous as virtually all phenotypes and most exposures typically classified as environmental have been found to be heritable. A polygenic score summarises the associations between millions of genetic variants and an outcome in a single value for each individual. Ever lowering costs have enabled the genotyping of many samples relevant to child psychology and psychiatry research, including cohort studies, leading to the proliferation of polygenic score studies. It is tempting to assume that associations detected between polygenic scores and phenotypes in those studies only reflect genetic effects. However, such associations can reflect many pathways (e.g. via environmental mediation) and biases. METHODS: Here, we provide a comprehensive overview of the many reasons why associations between polygenic scores, environmental exposures, and phenotypes exist. We include formal representations of common analyses in polygenic score studies using structural equation modelling. We derive biases, provide illustrative empirical examples and, when possible, mention steps that can be taken to alleviate those biases. RESULTS: Structural equation models and derivations show the many complexities arising from jointly modelling polygenic scores with environmental exposures and phenotypes. Counter-intuitive examples include that: (a) associations between polygenic scores and phenotypes may exist even in the absence of direct genetic effects; (b) associations between child polygenic scores and environmental exposures can exist in the absence of evocative/active gene-environment correlations; and (c) adjusting an exposure-outcome association for a polygenic score can increase rather than decrease bias. CONCLUSIONS: Strikingly, using polygenic scores may, in some cases, lead to more bias than not using them. Appropriately conducting and interpreting polygenic score studies thus requires researchers in child psychology and psychiatry and beyond to be versed in both epidemiological and genetic methods or build on interdisciplinary collaborations. En ligne : http://dx.doi.org/10.1111/jcpp.13607 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486 The p factor: genetic analyses support a general dimension of psychopathology in childhood and adolescence / Andrea G. ALLEGRINI in Journal of Child Psychology and Psychiatry, 61-1 (January 2020)
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PermalinkUsing DNA to predict behaviour problems from preschool to adulthood / Agnieszka GIDZIELA in Journal of Child Psychology and Psychiatry, 63-7 (July 2022)
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