Effects of DTNBP1 genotype on brain development in children / Stefania TOGNIN in Journal of Child Psychology and Psychiatry, 52-12 (December 2011)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 52-12 (December 2011) . - p.1287-1294 Titre : Effects of DTNBP1 genotype on brain development in children Type de document : Texte imprimé et/ou numérique Auteurs : Stefania TOGNIN, Auteur ; Essi VIDING, Auteur ; Eamon J. MCCRORY, Auteur ; Lauren J. TAYLOR, Auteur ; Michael C. O'DONOVAN, Auteur ; Philip MCGUIRE, Auteur ; Andrea MECHELLI, Auteur Année de publication : 2011 Article en page(s) : p.1287-1294 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Background:  Schizophrenia is a neurodevelopmental disorder, and risk genes are thought to act through disruption of brain development. Several genetic studies have identified dystrobrevin-binding protein 1 (DTNBP1, also known as dysbindin) as a potential susceptibility gene for schizophrenia, but its impact on brain development is poorly understood. The present investigation examined for the first time the effects of DTNBP1 on brain structure in children. Our hypothesis was that a genetic variation in DTNBP1 (i.e., the single nucleotide polymorphism rs2619538) would be associated with differences in both gray and white matter brain regions previously implicated in schizophrenia. Methods:  Magnetic resonance imaging and voxel-based morphometry were used to examine brain structure in 52 male children aged between 10 and 12 years. Statistical inferences on the effects of DTNBP1 genotype on gray and white matter volume (GMV and WMV) were made at p < .05 after family-wise error correction for multiple comparisons across the whole brain. Results:  Individuals homozygous for the schizophrenia high-risk allele (AA) compared with those homozygous for the low-risk allele (TT) expressed reduced GMV in the left anterior cingulate gyrus and reduced WMV in the left medial frontal area. Conclusions:  Our results suggest that genetic variation in DTNBP1 is associated with differences in gray and white matter; and that these effects are already evident in children as young as 10–12 years. These findings are consistent with the notion that the DTNBP1 genotype influences brain development and may thereby modulate vulnerability to schizophrenia. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2011.02427.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=147 [article] Effects of DTNBP1 genotype on brain development in children [Texte imprimé et/ou numérique] / Stefania TOGNIN, Auteur ; Essi VIDING, Auteur ; Eamon J. MCCRORY, Auteur ; Lauren J. TAYLOR, Auteur ; Michael C. O'DONOVAN, Auteur ; Philip MCGUIRE, Auteur ; Andrea MECHELLI, Auteur . - 2011 . - p.1287-1294. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 52-12 (December 2011) . - p.1287-1294 Index. décimale : PER Périodiques Résumé : Background:  Schizophrenia is a neurodevelopmental disorder, and risk genes are thought to act through disruption of brain development. Several genetic studies have identified dystrobrevin-binding protein 1 (DTNBP1, also known as dysbindin) as a potential susceptibility gene for schizophrenia, but its impact on brain development is poorly understood. The present investigation examined for the first time the effects of DTNBP1 on brain structure in children. Our hypothesis was that a genetic variation in DTNBP1 (i.e., the single nucleotide polymorphism rs2619538) would be associated with differences in both gray and white matter brain regions previously implicated in schizophrenia. Methods:  Magnetic resonance imaging and voxel-based morphometry were used to examine brain structure in 52 male children aged between 10 and 12 years. Statistical inferences on the effects of DTNBP1 genotype on gray and white matter volume (GMV and WMV) were made at p < .05 after family-wise error correction for multiple comparisons across the whole brain. Results:  Individuals homozygous for the schizophrenia high-risk allele (AA) compared with those homozygous for the low-risk allele (TT) expressed reduced GMV in the left anterior cingulate gyrus and reduced WMV in the left medial frontal area. Conclusions:  Our results suggest that genetic variation in DTNBP1 is associated with differences in gray and white matter; and that these effects are already evident in children as young as 10–12 years. These findings are consistent with the notion that the DTNBP1 genotype influences brain development and may thereby modulate vulnerability to schizophrenia. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2011.02427.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=147

Factor Structure of Autistic Traits in Children with ADHD / Joanna MARTIN in Journal of Autism and Developmental Disorders, 44-1 (January 2014)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 44-1 (January 2014) . - p.204-215 Titre : Factor Structure of Autistic Traits in Children with ADHD Type de document : Texte imprimé et/ou numérique Auteurs : Joanna MARTIN, Auteur ; Marian L. HAMSHERE, Auteur ; Michael C. O'DONOVAN, Auteur ; Michael RUTTER, Auteur ; Anita THAPAR, Auteur Article en page(s) : p.204-215 Langues : Anglais (eng) Mots-clés : ADHD  ASD  Factor analysis  Neurodevelopment Index. décimale : PER Périodiques Résumé : Attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) often co-occur. Factor analyses of ASD traits in children with and without ASD indicate the presence of social and restrictive–repetitive behaviour (RRB) factors. This study used exploratory factor analyses to determine the structure of ASD traits (assessed using the Social Communication Questionnaire) in children with ADHD. Distinct factors were observed for ‘social’ and ‘rigidity’ traits, corresponding to previous factor analyses in clinical ASD and population samples. This indicates that the split between social-communicative and RRB dimensions is unaffected by ADHD in children. Moreover, the study also finds that there is some overlap across hyperactive-impulsive symptoms and RRB traits in children with ADHD, which merits further investigation. En ligne : http://dx.doi.org/10.1007/s10803-013-1865-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=220 [article] Factor Structure of Autistic Traits in Children with ADHD [Texte imprimé et/ou numérique] / Joanna MARTIN, Auteur ; Marian L. HAMSHERE, Auteur ; Michael C. O'DONOVAN, Auteur ; Michael RUTTER, Auteur ; Anita THAPAR, Auteur . - p.204-215. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 44-1 (January 2014) . - p.204-215 Mots-clés : ADHD  ASD  Factor analysis  Neurodevelopment Index. décimale : PER Périodiques Résumé : Attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) often co-occur. Factor analyses of ASD traits in children with and without ASD indicate the presence of social and restrictive–repetitive behaviour (RRB) factors. This study used exploratory factor analyses to determine the structure of ASD traits (assessed using the Social Communication Questionnaire) in children with ADHD. Distinct factors were observed for ‘social’ and ‘rigidity’ traits, corresponding to previous factor analyses in clinical ASD and population samples. This indicates that the split between social-communicative and RRB dimensions is unaffected by ADHD in children. Moreover, the study also finds that there is some overlap across hyperactive-impulsive symptoms and RRB traits in children with ADHD, which merits further investigation. En ligne : http://dx.doi.org/10.1007/s10803-013-1865-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=220

Identifying mechanisms that underlie links between COMT genotype and aggression in male adolescents with ADHD / Stephanie H. M. VAN GOOZEN in Journal of Child Psychology and Psychiatry, 57-4 (April 2016)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 57-4 (April 2016) . - p.472-480 Titre : Identifying mechanisms that underlie links between COMT genotype and aggression in male adolescents with ADHD Type de document : Texte imprimé et/ou numérique Auteurs : Stephanie H. M. VAN GOOZEN, Auteur ; Kate LANGLEY, Auteur ; Clare NORTHOVER, Auteur ; Kelly HUBBLE, Auteur ; Katya RUBIA, Auteur ; Karen SCHEPMAN, Auteur ; Michael C. O'DONOVAN, Auteur ; Anita THAPAR, Auteur Article en page(s) : p.472-480 Langues : Anglais (eng) Mots-clés : ADHD  aggression  conduct disorder  COMT  genetic  child Index. décimale : PER Périodiques Résumé : Background There is a known strong genetic contribution to aggression in those with ADHD. In a previous investigation of a large population cohort, impaired ‘emotional/social cognitive’ processing, assessed by questionnaire, was observed to mediate the link between COMT Val158Met and aggression in individuals with ADHD. We set out to replicate and extend this finding in a clinical sample, using task-based and physiological assessments of emotional and cognitive processing. Our aim was to test the hypothesis that directly assessed emotional processing mediates the link between COMT Val158Met and aggression in young people with ADHD. Methods Males aged 10–17 years with ADHD were recruited from UK community clinics (n = 194). Research diagnostic interviews (parent and child) were used to assess psychopathology and generate DSM-IV Conduct Disorder symptom scores. Participants completed tasks assessing executive function (response inhibition and set shifting), empathy for fear, sadness and happiness, and fear conditioning [measured using skin conductance responses (SCR) to aversive stimuli]. Results COMT Val allele carriers showed poorer response inhibition (F = 5.27, p = .02) and set shifting abilities (F = 6.45, p = .01), reduced fear empathy (F = 4.33, p = .04) and reduced autonomic responsiveness (lower SCRs) to the conditioned aversive stimulus (F = 11.74, p = .001). COMT Val158Met did not predict impairments in recognising others' emotions or affective empathy for happiness or sadness. Mediation analysis revealed that impaired fear-related mechanisms indirectly mediated the link between COMT Val158Met and aggression. Conclusion Our findings suggest fear mechanisms as possible targets for psychological interventions to disrupt links between genetic risk and aggressive outcomes in ADHD. Our findings also reveal the potential of hypothesis-driven approaches for identifying neuropsychological mechanisms that mediate genetic risk effects on behaviour and psychopathology. En ligne : http://dx.doi.org/10.1111/jcpp.12464 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=285 [article] Identifying mechanisms that underlie links between COMT genotype and aggression in male adolescents with ADHD [Texte imprimé et/ou numérique] / Stephanie H. M. VAN GOOZEN, Auteur ; Kate LANGLEY, Auteur ; Clare NORTHOVER, Auteur ; Kelly HUBBLE, Auteur ; Katya RUBIA, Auteur ; Karen SCHEPMAN, Auteur ; Michael C. O'DONOVAN, Auteur ; Anita THAPAR, Auteur . - p.472-480. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 57-4 (April 2016) . - p.472-480 Mots-clés : ADHD  aggression  conduct disorder  COMT  genetic  child Index. décimale : PER Périodiques Résumé : Background There is a known strong genetic contribution to aggression in those with ADHD. In a previous investigation of a large population cohort, impaired ‘emotional/social cognitive’ processing, assessed by questionnaire, was observed to mediate the link between COMT Val158Met and aggression in individuals with ADHD. We set out to replicate and extend this finding in a clinical sample, using task-based and physiological assessments of emotional and cognitive processing. Our aim was to test the hypothesis that directly assessed emotional processing mediates the link between COMT Val158Met and aggression in young people with ADHD. Methods Males aged 10–17 years with ADHD were recruited from UK community clinics (n = 194). Research diagnostic interviews (parent and child) were used to assess psychopathology and generate DSM-IV Conduct Disorder symptom scores. Participants completed tasks assessing executive function (response inhibition and set shifting), empathy for fear, sadness and happiness, and fear conditioning [measured using skin conductance responses (SCR) to aversive stimuli]. Results COMT Val allele carriers showed poorer response inhibition (F = 5.27, p = .02) and set shifting abilities (F = 6.45, p = .01), reduced fear empathy (F = 4.33, p = .04) and reduced autonomic responsiveness (lower SCRs) to the conditioned aversive stimulus (F = 11.74, p = .001). COMT Val158Met did not predict impairments in recognising others' emotions or affective empathy for happiness or sadness. Mediation analysis revealed that impaired fear-related mechanisms indirectly mediated the link between COMT Val158Met and aggression. Conclusion Our findings suggest fear mechanisms as possible targets for psychological interventions to disrupt links between genetic risk and aggressive outcomes in ADHD. Our findings also reveal the potential of hypothesis-driven approaches for identifying neuropsychological mechanisms that mediate genetic risk effects on behaviour and psychopathology. En ligne : http://dx.doi.org/10.1111/jcpp.12464 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=285

Investigating attention-deficit hyperactivity disorder and autism spectrum disorder traits in the general population: What happens in adult life? / Lucy RIGLIN in Journal of Child Psychology and Psychiatry, 62-4 (April 2021)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 62-4 (April 2021) . - p.449-457 Titre : Investigating attention-deficit hyperactivity disorder and autism spectrum disorder traits in the general population: What happens in adult life? Type de document : Texte imprimé et/ou numérique Auteurs : Lucy RIGLIN, Auteur ; Beate LEPPERT, Auteur ; Kate LANGLEY, Auteur ; Ajay K. THAPAR, Auteur ; Michael C. O'DONOVAN, Auteur ; George DAVEY SMITH, Auteur ; Evie STERGIAKOULI, Auteur ; Kate TILLING, Auteur ; Anita THAPAR, Auteur Article en page(s) : p.449-457 Langues : Anglais (eng) Mots-clés : Avon Longitudinal Study of Parents and Children  Neurodevelopmental  adult  attention-deficit hyperactivity disorder  autism spectrum disorder  genetic Index. décimale : PER Périodiques Résumé : BACKGROUND: Attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are generally considered early-onset disorders so most research has therefore tended to focus on children. Differences between ADHD/ASD in adult life and childhood have been noted, but few population-based studies have examined them in adulthood. Furthermore, the interpretation of findings is hampered by changes in measure and from parent report to self-report. METHOD: We examined continuous/trait measures of parent- and self-rated ADHD and ASD in adulthood (age 25 years) in a UK prospective longitudinal sample ALPSAC (the Avon Longitudinal Study of Parents and Children), using many of the same measures that parents reported on in childhood (N = 6,064). Our aim was to investigate these traits in this population for mean-level sex differences, overlaps with other cognitive, learning and communication problems and their associations with polygenic risk scores (PRS) for neuropsychiatric disorders (ADHD, ASD, schizophrenia, depression and anxiety). RESULTS: ADHD and ASD traits in adulthood, as in childhood, showed associations with childhood cognitive, learning and communication problems and adult communication/language measures, although less so for self-ratings than parent-ratings. Males had higher ADHD and ASD trait levels, but this was not as marked as in childhood. In adulthood, ADHD (both parent- and self-rated) and ASD (parent-rated) symptoms showed associations with ADHD PRS; self-reported ADHD also showed association with depression PRS, whereas self-reported ASD did not show strong PRS associations. CONCLUSIONS: Our findings suggest that in young adults, ADHD and ASD symptoms have similar characteristics as they do in childhood. Associations with other cognitive, learning and communication problems, and ADHD PRS were somewhat less pronounced for self-reported adult ADHD and ASD symptoms, suggesting that even at age 25, parent reports, where available, could be clinically useful. En ligne : http://dx.doi.org/10.1111/jcpp.13297 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=445 [article] Investigating attention-deficit hyperactivity disorder and autism spectrum disorder traits in the general population: What happens in adult life? [Texte imprimé et/ou numérique] / Lucy RIGLIN, Auteur ; Beate LEPPERT, Auteur ; Kate LANGLEY, Auteur ; Ajay K. THAPAR, Auteur ; Michael C. O'DONOVAN, Auteur ; George DAVEY SMITH, Auteur ; Evie STERGIAKOULI, Auteur ; Kate TILLING, Auteur ; Anita THAPAR, Auteur . - p.449-457. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 62-4 (April 2021) . - p.449-457 Mots-clés : Avon Longitudinal Study of Parents and Children  Neurodevelopmental  adult  attention-deficit hyperactivity disorder  autism spectrum disorder  genetic Index. décimale : PER Périodiques Résumé : BACKGROUND: Attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are generally considered early-onset disorders so most research has therefore tended to focus on children. Differences between ADHD/ASD in adult life and childhood have been noted, but few population-based studies have examined them in adulthood. Furthermore, the interpretation of findings is hampered by changes in measure and from parent report to self-report. METHOD: We examined continuous/trait measures of parent- and self-rated ADHD and ASD in adulthood (age 25 years) in a UK prospective longitudinal sample ALPSAC (the Avon Longitudinal Study of Parents and Children), using many of the same measures that parents reported on in childhood (N = 6,064). Our aim was to investigate these traits in this population for mean-level sex differences, overlaps with other cognitive, learning and communication problems and their associations with polygenic risk scores (PRS) for neuropsychiatric disorders (ADHD, ASD, schizophrenia, depression and anxiety). RESULTS: ADHD and ASD traits in adulthood, as in childhood, showed associations with childhood cognitive, learning and communication problems and adult communication/language measures, although less so for self-ratings than parent-ratings. Males had higher ADHD and ASD trait levels, but this was not as marked as in childhood. In adulthood, ADHD (both parent- and self-rated) and ASD (parent-rated) symptoms showed associations with ADHD PRS; self-reported ADHD also showed association with depression PRS, whereas self-reported ASD did not show strong PRS associations. CONCLUSIONS: Our findings suggest that in young adults, ADHD and ASD symptoms have similar characteristics as they do in childhood. Associations with other cognitive, learning and communication problems, and ADHD PRS were somewhat less pronounced for self-reported adult ADHD and ASD symptoms, suggesting that even at age 25, parent reports, where available, could be clinically useful. En ligne : http://dx.doi.org/10.1111/jcpp.13297 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=445

Neurocognitive abilities in the general population and composite genetic risk scores for attention-deficit hyperactivity disorder / Joanna MARTIN in Journal of Child Psychology and Psychiatry, 56-6 (June 2015)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 56-6 (June 2015) . - p.648-656 Titre : Neurocognitive abilities in the general population and composite genetic risk scores for attention-deficit hyperactivity disorder Type de document : Texte imprimé et/ou numérique Auteurs : Joanna MARTIN, Auteur ; Marian L. HAMSHERE, Auteur ; Evangelia STERGIAKOULI, Auteur ; Michael C. O'DONOVAN, Auteur ; Anita THAPAR, Auteur Article en page(s) : p.648-656 Langues : Anglais (eng) Mots-clés : ALSPAC  ADHD  genetics  cognition Index. décimale : PER Périodiques Résumé : Background The genetic architecture of ADHD is complex, with rare and common variants involved. Common genetic variants (as indexed by a composite risk score) associated with clinical ADHD significantly predict ADHD and autistic-like behavioural traits in children from the general population, suggesting that ADHD lies at the extreme of normal trait variation. ADHD and other neurodevelopmental disorders share neurocognitive difficulties in several domains (e.g. impaired cognitive ability and executive functions). We hypothesised that ADHD composite genetic risk scores derived from clinical ADHD cases would also contribute to variation in neurocognitive abilities in the general population. Methods Children (N = 6,832) from a UK population cohort, the Avon Longitudinal Study of Parents and Children (ALSPAC), underwent neurocognitive testing. Parent-reported measures of their children's ADHD and autistic-like traits were used to construct a behavioural latent variable of ‘neurodevelopmental traits’. Composite genetic risk scores for ADHD were calculated for ALSPAC children based on findings from an independent ADHD case–control genome-wide association study. Structural equation modelling was used to assess associations between ADHD composite genetic risk scores and IQ, working memory, inhibitory control and facial emotion recognition, as well as the latent ‘neurodevelopmental trait’ measure. Results The results confirmed that neurocognitive and neurodevelopmental traits are correlated in children in the general population. Composite genetic risk scores for ADHD were independently associated with lower IQ (? = ?.05, p < .001) and working memory performance (? = ?.034, p = .013), even after accounting for the relationship with latent neurodevelopmental behavioural trait scores. No associations were found between composite genetic risk scores and inhibitory control or emotion recognition (p > .05). Conclusions These findings suggest that common genetic variants relevant to clinically diagnosed ADHD have pleiotropic effects on neurocognitive traits as well as behavioural dimensions in the general population. This further suggests that the well-recognised association between cognition and neurodevelopmental behavioural traits is underpinned at a biological level. En ligne : http://dx.doi.org/10.1111/jcpp.12336 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=260 [article] Neurocognitive abilities in the general population and composite genetic risk scores for attention-deficit hyperactivity disorder [Texte imprimé et/ou numérique] / Joanna MARTIN, Auteur ; Marian L. HAMSHERE, Auteur ; Evangelia STERGIAKOULI, Auteur ; Michael C. O'DONOVAN, Auteur ; Anita THAPAR, Auteur . - p.648-656. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 56-6 (June 2015) . - p.648-656 Mots-clés : ALSPAC  ADHD  genetics  cognition Index. décimale : PER Périodiques Résumé : Background The genetic architecture of ADHD is complex, with rare and common variants involved. Common genetic variants (as indexed by a composite risk score) associated with clinical ADHD significantly predict ADHD and autistic-like behavioural traits in children from the general population, suggesting that ADHD lies at the extreme of normal trait variation. ADHD and other neurodevelopmental disorders share neurocognitive difficulties in several domains (e.g. impaired cognitive ability and executive functions). We hypothesised that ADHD composite genetic risk scores derived from clinical ADHD cases would also contribute to variation in neurocognitive abilities in the general population. Methods Children (N = 6,832) from a UK population cohort, the Avon Longitudinal Study of Parents and Children (ALSPAC), underwent neurocognitive testing. Parent-reported measures of their children's ADHD and autistic-like traits were used to construct a behavioural latent variable of ‘neurodevelopmental traits’. Composite genetic risk scores for ADHD were calculated for ALSPAC children based on findings from an independent ADHD case–control genome-wide association study. Structural equation modelling was used to assess associations between ADHD composite genetic risk scores and IQ, working memory, inhibitory control and facial emotion recognition, as well as the latent ‘neurodevelopmental trait’ measure. Results The results confirmed that neurocognitive and neurodevelopmental traits are correlated in children in the general population. Composite genetic risk scores for ADHD were independently associated with lower IQ (? = ?.05, p < .001) and working memory performance (? = ?.034, p = .013), even after accounting for the relationship with latent neurodevelopmental behavioural trait scores. No associations were found between composite genetic risk scores and inhibitory control or emotion recognition (p > .05). Conclusions These findings suggest that common genetic variants relevant to clinically diagnosed ADHD have pleiotropic effects on neurocognitive traits as well as behavioural dimensions in the general population. This further suggests that the well-recognised association between cognition and neurodevelopmental behavioural traits is underpinned at a biological level. En ligne : http://dx.doi.org/10.1111/jcpp.12336 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=260

Predictors of developmental dyslexia in European orthographies with varying complexity / Karin LANDERL in Journal of Child Psychology and Psychiatry, 54-6 (June 2013)  

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Stratifying early-onset emotional disorders: using genetics to assess persistence in young people of European and South Asian ancestry / Joanna MARTIN ; Amy SHAKESHAFT ; Lucy RIGLIN ; Frances RICE ; Cathryn M. LEWIS ; Michael C. O'DONOVAN ; Anita THAPAR in Journal of Child Psychology and Psychiatry, 65-1 (January 2024)  

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The contribution of gene–environment interaction to psychopathology / Anita THAPAR in Development and Psychopathology, 19-4 (Fall 2007)  

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