26 results on '"Langley, Kate"'
Search Results
2. Sleep disturbances in ADHD: investigating the contribution of polygenic liability for ADHD and sleep-related phenotypes
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Lewis, Katie J. S., Martin, Joanna, Gregory, Alice M., Anney, Richard, Thapar, Anita, and Langley, Kate
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- 2022
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3. Investigating the associations between irritability and hot and cool executive functioning in those with ADHD
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Colonna, Silvia, Eyre, Olga, Agha, Sharifah Shameem, Thapar, Anita, van Goozen, Stephanie, and Langley, Kate
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- 2022
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4. Sex differences in attention‐deficit hyperactivity disorder diagnosis and clinical care: a national study of population healthcare records in Wales.
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Martin, Joanna, Langley, Kate, Cooper, Miriam, Rouquette, Olivier Y., John, Ann, Sayal, Kapil, Ford, Tamsin, and Thapar, Anita
- Abstract
Background Methods Results Conclusions Population‐based studies have observed sex biases in the diagnosis and treatment of attention‐deficit hyperactivity disorder (ADHD). Females are less likely to be diagnosed or prescribed ADHD medication. This study uses national healthcare records, to investigate sex differences in diagnosis and clinical care in young people with ADHD, particularly regarding recognition and treatment of other mental health conditions.The cohort included individuals diagnosed with ADHD, born between 1989 and 2013 and living in Wales between 2000 and 2019. Routine primary and secondary healthcare record data were used to derive diagnoses of ADHD and other neurodevelopmental and mental health conditions, as well as ADHD and antidepressant medications. Demographic variables included ethnicity, socioeconomic deprivation and contact with social services.There were 16,458 individuals diagnosed with ADHD (20.3% females, ages 3–30 years), with a male‐to‐female ratio of 3.9:1. Higher ratios (4.8:1) were seen in individuals diagnosed younger (<12 years), with the lowest ratio (1.9:1) in those diagnosed as adults (>18). Males were younger at first recorded ADHD diagnosis (mean = 10.9 vs. 12.6 years), more likely to be prescribed ADHD medication and younger at diagnosis of co‐occurring neurodevelopmental conditions. In contrast, females were more likely to receive a diagnosis of anxiety, depression or another mental health condition and to be prescribed antidepressant medications, prior to ADHD diagnosis. These sex differences were largely stable across demographic groups.This study adds to the evidence base that females with ADHD are experiencing later recognition and treatment of ADHD. The results indicate that this may be partly because of diagnostic overshadowing from other mental health conditions, such as anxiety and depression, or initial misdiagnosis. Further research and dissemination of findings to the public are needed to improve awareness, timely diagnosis and treatment of ADHD in females. [ABSTRACT FROM AUTHOR]
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- 2024
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5. Sleep disturbances in ADHD: investigating the contribution of polygenic liability for ADHD and sleep-related phenotypes.
- Author
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Lewis, Katie J. S., Martin, Joanna, Gregory, Alice M., Anney, Richard, Thapar, Anita, and Langley, Kate
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ATTENTION-deficit hyperactivity disorder ,SLEEP disorders ,RESEARCH funding ,PHENOTYPES ,COMORBIDITY - Abstract
Sleep disturbances are common in attention deficit hyperactivity disorder (ADHD) and associated with poor outcomes. We tested whether, in children with ADHD, (1) polygenic liability for sleep phenotypes is over- or under-transmitted from parents, (2) this liability is linked to comorbid sleep disturbances, and (3) ADHD genetic risk is associated with comorbid sleep disturbances. We derived polygenic scores (PGS) for insomnia, chronotype, sleep duration, and ADHD, in 758 children (5–18 years old) diagnosed with ADHD and their parents. We conducted polygenic transmission disequilibrium tests for each sleep PGS in complete parent–offspring ADHD trios (N = 328) and an independent replication sample of ADHD trios (N = 844). Next, we tested whether insomnia, sleep duration, and ADHD PGS were associated with co-occurring sleep phenotypes (hypersomnia, insomnia, restless sleep, poor sleep quality, and nightmares) in children with ADHD. Children's insomnia and chronotype PGS did not differ from mid-parent average PGS but long sleep duration PGS were significantly over-transmitted to children with ADHD. This was supported by a combined analysis using the replication sample. Insomnia, sleep duration, and ADHD PGS were not associated with comorbid sleep disturbances. There is weak evidence that children with ADHD over-inherit polygenic liability for longer sleep duration and do not differentially inherit polygenic liability for insomnia or chronotype. There was insufficient evidence that childhood sleep disturbances were driven by polygenic liability for ADHD or sleep traits, suggesting that sleep disturbances in ADHD may be aetiologically different to general population sleep phenotypes and do not index greater ADHD genetic risk burden. [ABSTRACT FROM AUTHOR]
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- 2023
- Full Text
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6. Maternal psychopathology and offspring clinical outcome: a four-year follow-up of boys with ADHD
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Agha, Sharifah Shameem, Zammit, Stanley, Thapar, Anita, and Langley, Kate
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- 2017
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7. Sex differences in anxiety and depression in children with ADHD:investigating genetic liability and comorbidity
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Martin, Joanna, Agha, Sharifah Shameem, Eyre, Olga, Riglin, Lucy, Langley, Kate, Hubbard, Leon, Stergiakouli , Evie, O'Donovan, Michael C, and Thapar, Anita
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sex differencesv ,polygenic risk scores ,anxiety disorders ,mental disorders ,depression ,ADHD ,ALSPAC ,behavioral disciplines and activities - Abstract
It is unknown why attention deficit hyperactivity disorder (ADHD) is more common in males, whereas anxiety and depression show a female population excess. We tested the hypothesis that anxiety and depression risk alleles manifest as ADHD in males. We also tested whether anxiety and depression in children with ADHD show a different etiology to typical anxiety and depression and whether this differs by sex. The primary clinical ADHD sample consisted of 885 (14% female) children. Psychiatric symptoms were assessed using standardized interviews. Polygenic risk scores (PRS) were derived using large genetic studies. Replication samples included independent clinical ADHD samples (N = 3,794; 25.7% female) and broadly defined population ADHD samples (N = 995; 33.4% female). We did not identify sex differences in anxiety or depression PRS in children with ADHD. In the primary sample, anxiety PRS were associated with social and generalized anxiety in males, with evidence of a sex-by-PRS interaction for social anxiety. These results did not replicate in the broadly defined ADHD sample. Depression PRS were not associated with comorbid depression symptoms. The results suggest that anxiety and depression genetic risks are not more likely to lead to ADHD in males. Also, the evidence for shared etiology between anxiety symptoms in those with ADHD and typical anxiety was weak and needs replication.
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- 2021
8. Autistic traits in children with ADHD index clinical and cognitive problems
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Cooper, Miriam, Martin, Joanna, Langley, Kate, Hamshere, Marian, and Thapar, Anita
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- 2014
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9. Risk variants and polygenic architecture of disruptive behavior disorders in the context of attention-deficit/hyperactivity disorder
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Demontis, Ditte, Walters, Raymond K., Rajagopal, Veera M., Waldman, Irwin D., Grove, Jakob, Als, Thomas D., Dalsgaard, Søren, Ribasas, Marta, Bybjerg-Grauholm, Jonas, Bækvad-Hansen, Maria, Werge, Thomas, Nordentoft, Merete, Mors, Ole, Mortensen, Preben Bo, (PGC), ADHD Working Group of the Psychiatric Genomics Consortium, Andreassen, Ole A., Arranz, Maria Jesús, Banaschewski, Tobias, Bau, Claiton, Bellgrove, Mark, Biederman, Joseph, Brikell, Isabell, Buitelaar, Jan K., Burton, Christie L., Casas, Miguel, Crosbie, Jennifer, Doyle, Alysa E., Ebstein, Richard P., Elia, Josephine, Elizabeth, Corfield C., Grevet, Eugenio, Grizenko, Natalie, Havdahl, Alexandra, Hawi, Ziarih, Hebebrand, Johannes, Hervas, Amaia, Hohmann, Sarah, Haavik, Jan, Joober, Ridha, Kent, Lindsey, Kuntsi, Jonna, Langley, Kate, Larsson, Henrik, Lesch, Klaus-Peter, Leung, Patrick W. L., Liao, Calwing, Loo, Sandra K., Martin, Joanna, Martin, Nicholas G., Medland, Sarah E., Miranda, Ana, Mota, Nina Roth, Oades, Robert D., Ramos-Quiroga, Josep Antoni, Reif, Andreas, Rietschel, Marcella, Roeyers, Herbert, Rohde, Luis Augusto, Rothenberger, Aribert, Rovira, Paula, Sánchez-Mora, Cristina, Schachar, Russell James, Sengupta, Sarojini, Artigas, Maria Soler, Steinhausen, Hans-Christoph, Thapar, Anita, Witt, Stephanie H., Yang, Li, Zayats, Tetyana, Zhang-James, Yanli, Cormand, Bru, Hougaard, David M., Neale, Benjamin M., Franke, Barbara, Faraone, Stephen V., Børglum, Anders D., University of St Andrews. School of Medicine, University of St Andrews. Institute of Behavioural and Neural Sciences, University of St Andrews. Cellular Medicine Division, Institut Català de la Salut, [Demontis D, Rajagopal VM, Als TD] The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Aarhus, Denmark. Center for Genomics and Personalized Medicine, Aarhus, Denmark. Department of Biomedicine - Human Genetics, Aarhus University, Aarhus, Denmark. [Walters RK] Analytic and Translational Genetics Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA, USA. [Waldman ID] Department of Psychology, Emory University, Atlanta, GA, USA. [Grove J] The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Aarhus, Denmark. Center for Genomics and Personalized Medicine, Aarhus, Denmark. Department of Biomedicine - Human Genetics, Aarhus University, Aarhus, Denmark. [Ribasés M] Unitat de Psiquiatria Genètica, Grup de recerca en Psiquiatria, salut mental i addiccions, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain. Servei de Psiquiatria, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Biomedical Network Research Center on Mental Health (CIBERSAM), Instituto de Salud Carlos III, Madrid, Spain. Departament de Genètica, Microbiologia i Estadística, Facultat de Biologia, Universitat de Barcelona, Barcelona, Catalonia, Spain, and Vall d'Hebron Barcelona Hospital Campus
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Male ,0301 basic medicine ,Multifactorial Inheritance ,Trastorns per dèficit d'atenció amb hiperactivitat en els infants ,Medizin ,General Physics and Astronomy ,Genome-wide association study ,Comorbidity ,Genome-wide association studies ,Attention deficit disorder with hyperactivity in children ,conducta y mecanismos de la conducta::conducta::conducta y mecanismos de la conducta::conducta::conducta infantil::conducta problemática [PSIQUIATRÍA Y PSICOLOGÍA] ,Cohort Studies ,0302 clinical medicine ,Mental Disorders::Neurodevelopmental Disorders::Attention Deficit and Disruptive Behavior Disorders::Attention Deficit Disorder with Hyperactivity [PSYCHIATRY AND PSYCHOLOGY] ,Risk Factors ,2.1 Biological and endogenous factors ,Medicine ,Attention Deficit Disorder with Hyperactivity/epidemiology ,Aetiology ,Child ,China/epidemiology ,Violence Research ,Pediatric ,Multidisciplinary ,Genetic Predisposition to Disease/genetics ,Attention Deficit and Disruptive Behavior Disorders/epidemiology ,Single Nucleotide ,3. Good health ,Europe ,Mental Health ,Attention Deficit and Disruptive Behavior Disorders ,Cohort ,Genome-Wide Association Study/methods ,Attention Deficit Disorder (ADD) ,Female ,medicine.symptom ,RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry ,Clinical psychology ,China ,Investigative Techniques::Epidemiologic Methods::Epidemiologic Research Design::Genome-Wide Association Study [ANALYTICAL, DIAGNOSTIC AND THERAPEUTIC TECHNIQUES, AND EQUIPMENT] ,Science ,Context (language use) ,Locus (genetics) ,QH426 Genetics ,Polymorphism, Single Nucleotide ,behavioral disciplines and activities ,Article ,General Biochemistry, Genetics and Molecular Biology ,Europe/epidemiology ,03 medical and health sciences ,Aggressiveness in children ,Behavioral and Social Science ,mental disorders ,Genetics ,ADHD ,Humans ,SNP ,Attention deficit hyperactivity disorder ,Genetic Predisposition to Disease ,Polymorphism ,Author Correction ,QH426 ,Multifactorial Inheritance/genetics ,Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7] ,business.industry ,Aggression ,Prevention ,Human Genome ,DAS ,General Chemistry ,Agressivitat en els infants ,Heritability ,medicine.disease ,Attention Deficit Hyperactivity Disorder (ADHD) ,Behavior and Behavior Mechanisms::Behavior::Behavior and Behavior Mechanisms::Behavior::Child Behavior::Problem Behavior [PSYCHIATRY AND PSYCHOLOGY] ,Brain Disorders ,Genòmica ,ADHD Working Group of the Psychiatric Genomics Consortium ,Trastorn per dèficit d'atenció amb hiperactivitat ,030104 developmental biology ,Attention Deficit Disorder with Hyperactivity ,técnicas de investigación::métodos epidemiológicos::diseño de la investigación epidemiológica::estudio de asociación genómica completa [TÉCNICAS Y EQUIPOS ANALÍTICOS, DIAGNÓSTICOS Y TERAPÉUTICOS] ,RC0321 ,trastornos mentales::trastornos del desarrollo neurológico::trastornos conductuales disruptivos y déficit de atención::trastornos de déficit de atención con hiperactividad [PSIQUIATRÍA Y PSICOLOGÍA] ,business ,030217 neurology & neurosurgery ,Genome-Wide Association Study - Abstract
Attention-Deficit/Hyperactivity Disorder (ADHD) is a childhood psychiatric disorder often comorbid with disruptive behavior disorders (DBDs). Here, we report a GWAS meta-analysis of ADHD comorbid with DBDs (ADHD + DBDs) including 3802 cases and 31,305 controls. We identify three genome-wide significant loci on chromosomes 1, 7, and 11. A meta-analysis including a Chinese cohort supports that the locus on chromosome 11 is a strong risk locus for ADHD + DBDs across European and Chinese ancestries (rs7118422, P = 3.15×10−10, OR = 1.17). We find a higher SNP heritability for ADHD + DBDs (h2SNP = 0.34) when compared to ADHD without DBDs (h2SNP = 0.20), high genetic correlations between ADHD + DBDs and aggressive (rg = 0.81) and anti-social behaviors (rg = 0.82), and an increased burden (polygenic score) of variants associated with ADHD and aggression in ADHD + DBDs compared to ADHD without DBDs. Our results suggest an increased load of common risk variants in ADHD + DBDs compared to ADHD without DBDs, which in part can be explained by variants associated with aggressive behavior., ADHD is often found to be comorbid with disruptive behavior disorders, but the genetic loci underlying this comorbidity are unknown. Here, the authors have performed a GWAS meta-analysis of ADHD with disruptive behavior disorders, finding three genome-wide significant loci in Europeans, and replicating one in a Chinese cohort.
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- 2021
10. "Late-onset" ADHD symptoms in young adulthood: Is this ADHD?
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Riglin, Lucy, Wootton, Robyn E., Livingston, Lucy A., Agnew-Blais, Jessica, Arseneault, Louise, Blakey, Rachel, Agha, Sharifah Shameem, Langley, Kate, Collishaw, Stephan, O'Donovan, Michael C., Davey Smith, George, Stergiakouli, Evie, Tilling, Kate, and Thapar, Anita
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YOUNG adults ,ATTENTION-deficit hyperactivity disorder ,MONOGENIC & polygenic inheritance (Genetics) ,TASK performance ,COGNITIVE ability - Abstract
Objective: We investigated whether "late-onset" ADHD that emerges in adolescence/adulthood is similar in risk factor profile to: (1) child-onset ADHD, but emerges later because of scaffolding/compensation from childhood resources; and (2) depression, because it typically onsets in adolescence/adulthood and shows symptom and genetic overlaps with ADHD. Methods: We examined associations between late-onset ADHD and ADHD risk factors, cognitive tasks, childhood resources and depression risk factors in a population-based cohort followed-up to age 25 years (N =4224–9764). Results: Parent-rated late-onset ADHD was like child-onset persistent ADHD in associations with ADHD polygenic risk scores and cognitive task performance, although self-rated late-onset ADHD was not. Late-onset ADHD was associated with higher levels of childhood resources than child-onset ADHD and did not show strong evidence of association with depression risk factors. Conclusions: Late-onset ADHD shares characteristics with child-onset ADHD when parent-rated, but differences for self-reports require investigation. Childhood resources may delay the onset of ADHD. [ABSTRACT FROM AUTHOR]
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- 2022
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11. Are parental ADHD problems associated with a more severe clinical presentation and greater family adversity in children with ADHD?
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Agha, Sharifah Shameem, Zammit, Stanley, Thapar, Anita, and Langley, Kate
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- 2013
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12. Molecular genetic contribution to the developmental course of attention-deficit hyperactivity disorder
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Langley, Kate, Fowler, Tom A., Grady, Deborah L., Moyzis, Robert K., Holmans, Peter A., van den Bree, Marianne B. M., Owen, Michael J., O’Donovan, Michael C., and Thapar, Anita
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- 2009
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13. Identifying mechanisms that underlie links between COMT genotype and aggression in male adolescents with ADHD
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van Goozen, Stephanie H. M., Langley, Kate, Northover, Clare, Hubble, Kelly, Rubia, Katya, Schepman, Karen, O'Donovan, Michael C., and Thapar, Anita
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Male ,child ,conduct disorder ,Adolescent ,Genotype ,aggression ,Emotions ,BF ,Original Articles ,Fear ,Catechol O-Methyltransferase ,behavioral disciplines and activities ,COMT ,Executive Function ,Inhibition, Psychological ,mental disorders ,RC0321 ,ADHD ,Humans ,Original Article ,genetic ,Empathy - Abstract
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.
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- 2015
14. Emotion Regulation in Adolescent Males with Attention-Deficit Hyperactivity Disorder: Testing the Effects of Comorbid Conduct Disorder
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Northover, Clare, Thapar, Anita, Langley, Kate, and van Goozen, Stephanie
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emotion regulation ,conduct disorder ,ultimatum game ,mental disorders ,aggression ,BF ,ADHD ,callous-unemotional traits ,R1 ,lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry ,Article ,lcsh:RC321-571 - Abstract
Although attention-deficit hyperactivity disorder (ADHD) has been linked to emotion dysregulation, few studies have experimentally investigated this whilst controlling for the effects of comorbid conduct disorder (CD). Economic decision-making games that assess how individuals respond to offers varying in fairness have been used to study emotion regulation. The present study compared adolescent boys with ADHD (n = 90), ADHD + CD (n = 94) and typical controls (n = 47) on the Ultimatum Game and examined the contribution of ADHD and CD symptom scores and callous and unemotional traits to acceptance levels of unfair offers. There were no significant differences in acceptance rates of fair and highly unfair offers between groups, and only boys with ADHD did not significantly differ from the controls. However, the subgroup of boys with ADHD and additional high levels of aggressive CD symptoms rejected significantly more ambiguous (i.e., moderately unfair) offers than any other subgroup, suggesting impaired emotion regulation in those with ADHD and aggressive CD. Correlations within the CD group showed that the rejection rate to moderately unfair offers was predicted by aggressive CD symptom severity, but not callous and unemotional traits. These findings highlight the fact that ADHD is a heterogeneous condition from an emotion regulation point of view.
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- 2015
15. Assessment of age-at-onset criterion for adult attention-deficit hyperactivity disorder.
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Riglin, Lucy, Blakey, Rachel, Langley, Kate, Thapar, Ajay K., Agha, Sharifah Shameem, Davey Smith, George, Stergiakouli, Evie, and Thapar, Anita
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ATTENTION-deficit hyperactivity disorder ,RECEIVER operating characteristic curves - Abstract
To investigate the accuracy of the age-at-onset criterion in those who meet other DSM-5 criteria for attention-deficit hyperactivity disorder, using a prospective population cohort we compared four different approaches to asking those aged 25 years (n = 138) when their symptoms started. Receiver operating characteristic curves showed variation between the approaches (χ(3) = 8.99, P = 0.03); all four showed low discrimination against symptoms that had been assessed when they were children (area under the curve: 0.57-0.68). Asking adults to recall specific symptoms may be preferable to recalling at what age symptoms started. However, limitations to retrospective recall add to debate on the validity of ADHD age-at-onset assessment. [ABSTRACT FROM AUTHOR]
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- 2022
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16. Parent Psychopathology and Neurocognitive Functioning in Children With ADHD.
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Agha, Sharifah Shameem, Zammit, Stanley, Thapar, Anita, and Langley, Kate
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NEUROBEHAVIORAL disorders ,PATHOLOGICAL psychology ,CHILDREN with attention-deficit hyperactivity disorder ,SHORT-term memory ,COGNITION disorders ,RESEARCH ,RESEARCH methodology ,COGNITION ,MEDICAL cooperation ,EVALUATION research ,ATTENTION-deficit hyperactivity disorder ,NEUROPSYCHOLOGICAL tests ,COMPARATIVE studies ,ATTENTION ,PARENTS - Abstract
Objective: The objective of this study was to examine the association between parent mental health (ADHD and depression) and offspring performance on neurocognitive tasks in children with ADHD. Method: The clinical sample consisted of 570 children (85% males, mean age: 10.77 years) with ADHD who completed neurocognitive tasks measuring working memory, attention set-shifting, and motivational deficits. Questionnaire measures were used to assess ADHD and depression symptom presence in parents. Results: Controlling for ADHD severity, children of parents with ADHD had poorer working memory (B = -0.25, 95% confidence interval [CI] [-0.45, -0.07], p = .01) and increased errors on the extra dimensional shift stage of the set-shifting task (B = 0.26 95% CI [0.02, 0.50], p = .04). Parent depression was not associated with offspring performance on any of the assessed neurocognitive tasks. Conclusion: Children with ADHD who have a parent with ADHD symptom presence are a subgroup of children who may have additional neurocognitive impairments that have potential implications when implementing interventions that target cognition and learning. [ABSTRACT FROM AUTHOR]
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- 2020
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17. Irritability in ADHD: Associations with depression liability
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Eyre, Olga, Langley, Kate, Stringaris, Argyris, Leibenluft, Ellen, Collishaw, Stephan, and Thapar, Anita
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DMDD ,Depression ,RC0321 ,ADHD ,Irritability - Abstract
Background Irritability and the new DSM-5 diagnostic category of Disruptive Mood Dysregulation Disorder (DMDD) have been conceptualised as related to mood disorder. Irritability is common in Attention Deficit Hyperactivity Disorder (ADHD) but little is known about its association with depression risk in this group. This study aims to establish levels of irritability and prevalence of DMDD in a clinical sample of children with ADHD, and examine their association with anxiety, depression and family history of depression. Methods The sample consisted of 696 children (mean age 10.9 years) with a diagnosis of ADHD, recruited from UK child psychiatry and paediatric clinics. Parents completed the Child and Adolescent Psychiatric Assessment, a semi-structured diagnostic interview, about their child. This was used to establish prevalence of DMDD, anxiety disorder and depressive disorder, as well as obtain symptom scores for irritability, anxiety and depression. Questionnaires assessed current parental depression, and family history of depression. Result Irritability was common, with 91% endorsing at least one irritable symptom. 3-month DMDD prevalence was 31%. Children with higher levels of irritability or DMDD were more likely to have comorbid symptoms of anxiety, depression and a family history of depression. Limitations Results are based on a clinical sample, so may not be generalizable to children with ADHD in the general population. Conclusions Irritability and DMDD were common, and were associated with markers of depression liability. Longitudinal studies are needed to examine the association between irritability and depression in youth with ADHD as they get older.
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- 2017
18. Maternal psychopathology and offspring clinical outcome:a four year follow-up of boys with ADHD European Child & Adolescent Psychiatry
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Agha, Sharifah Shameem, Zammit, Stan, Thapar, Anita, and Langley, Kate
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Mother self-reported ADHD ,mental disorders ,ADHD ,Conduct disorder symptoms ,Mother self-reported depression ,behavioral disciplines and activities - Abstract
Previous cross-sectional research has shown that parents of children with attention deficit hyperactivity disorder (ADHD) have high rates of psychopathology, especially ADHD and depression. However, it is not clear whether different types of parent psychopathology contribute to the course and persistence of ADHD in the child over time. The aim of this two wave study was to investigate if mother self-reported ADHD and depression influence persistence of offspring ADHD and conduct disorder symptom severity in adolescents diagnosed with ADHD in childhood. A sample of 143 males with a confirmed diagnosis of ADHD participated in this study. ADHD and conduct disorder symptoms were assessed at baseline and reassessed 4 years later. The boys in this sample had a mean age of 10.7 years at Time 1 (SD 2.14, range 6–15 years) and 13.73 years at Time 2 (SD 1.74, range 10–17 years). Questionnaire measures were used to assess ADHD and depression symptoms in mothers at Time 1. Mother self-reported ADHD was not associated with a change in child ADHD or conduct symptom severity over time. Mother self-reported depression was found to predict an increase in child conduct disorder symptoms, but did not contribute to ADHD symptom levels. This study provides the first evidence that concurrent depression in mothers may be a predictor of worsening conduct disorder symptoms in adolescents with ADHD. It may, therefore, be important to screen for depression in mothers of children with ADHD in clinical practice to tailor interventions accordingly.
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- 2017
19. Cortisol levels at baseline and under stress in adolescent males with Attention-Deficit Hyperactivity Disorder, with or without comorbid Conduct Disorder
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Northover, Clare, Thapar, Anita, Langley, Kate, Fairchild, Graeme, and van Goozen, Stephanie H.M.
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Psychiatry and Mental health ,Callous-unemotional traits ,mental disorders ,ADHD ,Stress ,behavioral disciplines and activities ,Biological Psychiatry ,Cortisol ,Conduct disorder - Abstract
Reported findings on cortisol reactivity to stress in young people with ADHD are very variable. This inconsistency may be explained by high rates of comorbidity with Conduct Disorder (CD). The present study examined cortisol responses to a psychosocial stressor in a large sample of adolescent males with ADHD (n=202), with or without a comorbid diagnosis of Conduct Disorder (CD). Associations between stress reactivity and callous-unemotional traits and internalizing symptoms were also assessed. The ADHD only (n=95) and ADHD+CD (n=107) groups did not differ in baseline cortisol, but the ADHD+CD group showed significantly reduced cortisol stress reactivity relative to the ADHD only group. Regression analyses indicated that ADHD symptom severity predicted reduced baseline cortisol, whereas CD symptom severity predicted increased baseline cortisol (ADHD β=−0.24, CD β=0.16, R=0.26) and reduced cortisol stress reactivity (β=−0.17, R=0.17). Callous-unemotional traits and internalizing symptoms were not significantly related to baseline or stress-induced cortisol. Impaired cortisol reactivity is hypothesised to reflect fearlessness and is associated with deficient emotion regulation and inhibition of aggressive and antisocial behaviour. Consequently, it may partly explain the greater severity of problems seen in those with comorbid ADHD and CD.
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- 2016
20. Identifying mechanisms that underlie links between COMT genotype and aggression in male adolescents with ADHD
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van Goozen, Stephanie H M, Langley, Kate, Northover, Clare, Hubble, Kelly, Rubia, Katya, Schepman, Karen, O'Donovan, Michael C., and Thapar, Anita
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Aggression ,Genetic ,ADHD ,Child ,COMT ,Conduct disorder - Published
- 2016
21. Identifying mechanisms that underlie links between COMT genotype and aggression in male adolescents with ADHD.
- Author
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Goozen, Stephanie H.M., Langley, Kate, Northover, Clare, Hubble, Kelly, Rubia, Katya, Schepman, Karen, O'Donovan, Michael C., and Thapar, Anita
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GENETICS of aggression , *ADOLESCENT psychology , *ALLELES , *ANALYSIS of variance , *ANXIETY , *ATTENTION-deficit hyperactivity disorder , *BEHAVIOR disorders in children , *STATISTICAL correlation , *EMOTIONS , *EMPATHY , *FEAR , *GENETIC polymorphisms , *INTELLIGENCE tests , *INTERVIEWING , *SENSORY perception , *PROBABILITY theory , *PATHOLOGICAL psychology , *QUESTIONNAIRES , *RESEARCH funding , *TASK performance , *EXECUTIVE function , *DATA analysis software , *GENOTYPES - Abstract
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 V al 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. [ABSTRACT FROM AUTHOR]
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- 2016
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22. Practitioner Review: What have we learnt about the causes of ADHD?
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Thapar, Anita, Cooper, Miriam, Eyre, Olga, and Langley, Kate
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ATTENTION-deficit hyperactivity disorder ,AUTISM ,MATERNAL-fetal exchange ,MEDLINE ,ONLINE information services ,RESEARCH funding ,SYSTEMATIC reviews ,COMORBIDITY ,ENVIRONMENTAL exposure ,HOME environment ,GENETICS - Abstract
Background: Attention deficit hyperactivity disorder (ADHD) and its possible causes still attract controversy. Genes, pre and perinatal risks, psychosocial factors and environmental toxins have all been considered as potential risk factors. Method: This review (focussing on literature published since 1997, selected from a search of PubMed) critically considers putative risk factors with a focus on genetics and selected environmental risks, examines their relationships with ADHD and discusses the likelihood that these risks are causal as well as some of the main implications. Results: No single risk factor explains ADHD. Both inherited and noninherited factors contribute and their effects are interdependent. ADHD is familial and heritable. Research into the inherited and molecular genetic contributions to ADHD suggest an important overlap with other neurodevelopmental problems, notably, autism spectrum disorders. Having a biological relative with ADHD, large, rare copy number variants, some small effect size candidate gene variants, extreme early adversity, pre and postnatal exposure to lead and low birth weight/prematurity have been most consistently found as risk factors, but none are yet known to be definitely causal. There is a large literature documenting associations between ADHD and a wide variety of putative environmental risks that can, at present, only be regarded as correlates. Findings from research designs that go beyond simply testing for association are beginning to contest the robustness of some environmental exposures previously thought to be ADHD risk factors. Conclusions: The genetic risks implicated in ADHD generally tend to have small effect sizes or be rare and often increase risk of many other types of psychopathology. Thus, they cannot be used for prediction, genetic testing or diagnostic purposes beyond what is predicted by a family history. There is a need to consider the possibility of parents and siblings being similarly affected and how this might impact on engagement with families, influence interventions and require integration with adult services. Genetic contributions to disorder do not necessarily mean that medications are the treatment of choice. We also consider how findings might influence the conceptualisation of ADHD, public health policy implications and why it is unhelpful and incorrect to dichotomise genetic/biological and environmental explanations. It is essential that practitioners can interpret genetic and aetiological research findings and impart informed explanations to families. [ABSTRACT FROM AUTHOR]
- Published
- 2013
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23. Five Years On: Public Sector Service Use Related to Mental Health in Young People with ADHD or Hyperkinetic Disorder Five Years After Diagnosis.
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Ford, Tamsin, Fowler, Tom, Langley, Kate, Whittinger, Naureen, and Thapar, Anita
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ATTENTION-deficit hyperactivity disorder ,MENTAL health ,OPERANT behavior ,YOUNG adult psychology ,BEHAVIOR disorders in children ,CHILDREN with attention-deficit hyperactivity disorder ,CHILD psychology research ,PSYCHIATRIC research ,PSYCHOPHARMACOLOGY - Abstract
Background: Little is known about ongoing service use among young people with ADHD, but this information is important to the development of services to support these young people. Methods: A cohort of young people with ADHD or hyperkinetic disorder ( n = 115) was followed up five to seven years after diagnosis. Details are presented of their use of public sector services over the 12 months preceding reassessment, compared to young people with ADHD from a large epidemiological study. Results: Most children remained in contact with CAMHS, with high rates of contact with schools, educational professionals and the criminal justice system. Nearly all had taken medication at some point, while many still were using it. There were low reported rates of psychological and group interventions within the last twelve months, but this does not rule out earlier access to such treatments. Conclusions: Children with ADHD utilise long-term support from public sector services, and cross agency strategies or clinics may help to optimise functioning. [ABSTRACT FROM AUTHOR]
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- 2008
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24. Investigating Direct and Indirect Genetic Effects in Attention-Deficit/Hyperactivity Disorder Using Parent-Offspring Trios.
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Martin, Joanna, Wray, Matthew, Agha, Sharifah Shameem, Lewis, Katie J.S., Anney, Richard J.L., O'Donovan, Michael C., Thapar, Anita, and Langley, Kate
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- *
ATTENTION-deficit hyperactivity disorder , *DISEASE risk factors , *BIRTHPARENTS , *TOURETTE syndrome , *MONOGENIC & polygenic inheritance (Genetics) - Abstract
Attention-deficit/hyperactivity disorder (ADHD) is highly heritable, but little is known about the relative effects of transmitted (i.e., direct) and nontransmitted (i.e., indirect) common variant risks. Using parent-offspring trios, we tested whether polygenic liability for neurodevelopmental and psychiatric disorders and lower cognitive ability is overtransmitted to ADHD probands. We also tested for indirect or genetic nurture effects by examining whether nontransmitted ADHD polygenic liability is elevated. Finally, we examined whether complete trios are representative of the clinical ADHD population. Polygenic risk scores (PRSs) for ADHD, anxiety, autism, bipolar disorder, depression, obsessive-compulsive disorder, schizophrenia, Tourette syndrome, and cognitive ability were calculated in UK control subjects (n = 5081), UK probands with ADHD (n = 857), their biological parents (n = 328 trios), and also a replication sample of 844 ADHD trios. ADHD PRSs were overtransmitted and cognitive ability and obsessive-compulsive disorder PRSs were undertransmitted. These results were independently replicated. Overtransmission of polygenic liability was not observed for other disorders. Nontransmitted alleles were not enriched for ADHD liability compared with control subjects. Probands from incomplete trios had more hyperactive-impulsive and conduct disorder symptoms, lower IQ, and lower socioeconomic status than complete trios. PRS did not vary by trio status. The results support direct transmission of polygenic liability for ADHD and cognitive ability from parents to offspring, but not for other neurodevelopmental/psychiatric disorders. They also suggest that nontransmitted neurodevelopmental/psychiatric parental alleles do not contribute indirectly to ADHD via genetic nurture. Furthermore, ascertainment of complete ADHD trios may be nonrandom, in terms of demographic and clinical factors. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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25. Prenatal Smoking Might Not Cause Attention-Deficit/Hyperactivity Disorder: Evidence from a Novel Design
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Thapar, Anita, Rice, Frances, Hay, Dale, Boivin, Jacky, Langley, Kate, van den Bree, Marianne, Rutter, Michael, and Harold, Gordon
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- *
WOMEN'S tobacco use , *PREGNANT women , *PRENATAL influences , *RISK factors of attention-deficit hyperactivity disorder , *SCIENTIFIC observation , *SYMPTOMS , *HEREDITY , *REPRODUCTIVE technology - Abstract
Background: It is widely considered that exposure to maternal cigarette smoking in pregnancy has risk effects on offspring attention-deficit/hyperactivity disorder (ADHD). This view is supported by consistent observations of association. It is, however, impossible to be certain of adequate control for confounding factors with observational designs. We use a novel “natural experiment” design that separates prenatal environmental from alternative inherited effects. Methods: The design is based on offspring conceived with Assisted Reproductive Technologies recruited from 20 fertility clinics in the United Kingdom and United States who were: 1) genetically unrelated, and 2) related to the woman who underwent the pregnancy. If maternal smoking in pregnancy has true risk effects, association will be observed with ADHD regardless of whether mother and offspring are related or unrelated. Data were obtained from 815 families of children ages 4 years–11 years with parent questionnaires and antenatal records. Birth weight was used as a comparison outcome. The key outcome considered was child ADHD symptoms. Results: Association between smoking in pregnancy and lower birth weight was found in unrelated and related mother-offspring pairs, consistent with a true risk effect. However, for ADHD symptoms, the magnitude of association was significantly higher in the related pairs (β = .102, p < .02) than in the unrelated pairs (β= −.052, p > .10), suggesting inherited effects. Conclusions: Our findings highlight the need to test causal hypotheses with genetically sensitive designs. Inherited confounds are not necessarily removed by statistical controls. The previously observed association between maternal smoking in pregnancy and ADHD might represent an inherited effect. [Copyright &y& Elsevier]
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- 2009
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26. Investigating the validity of the Strengths and Difficulties Questionnaire to assess ADHD in young adulthood.
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Riglin, Lucy, Agha, Sharifah Shameem, Eyre, Olga, Bevan Jones, Rhys, Wootton, Robyn E, Thapar, Ajay K, Collishaw, Stephan, Stergiakouli, Evie, Langley, Kate, and Thapar, Anita
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- *
YOUNG adults , *ATTENTION-deficit hyperactivity disorder , *QUESTIONNAIRES - Abstract
• The SDQ is widely used to assess ADHD symptoms in children. • We investigated the validity of the SDQ to assess ADHD at age 25 years. • The SDQ ADHD subscale had high validity in distinguishing DSM-5 ADHD cases from non-cases. • A lower cut-point is needed to identify ADHD diagnosis in young adulthood compared to younger ages. • The SDQ is appropriate for ADHD research across different development periods. Attention Deficit Hyperactivity Disorder (ADHD) symptoms typically onset early and persist into adulthood for many. Robust investigation of symptom continuity and discontinuity requires repeated assessments using the same measure, but research is lacking into whether measures used to assess ADHD symptoms in childhood are also valid in adulthood. The Strengths and Difficulties Questionnaire (SDQ) is widely used to assess ADHD symptoms in children, but little is known about its utility in adulthood. The aim of this study was to assess the validity of the SDQ hyperactivity/ADHD subscale to distinguish between cases and non-cases of DSM-5 ADHD at age 25 years in a UK population cohort (N = 4121). ADHD diagnosis was derived using the Barkley Adult ADHD Rating Scale-IV. Analyses suggested that the self-rated SDQ ADHD subscale had high validity in distinguishing ADHD cases/non-cases in young adulthood (area under the curve=0.90, 95% CI=0.87–0.93) and indicated a lower cut-point for identifying those who may have an ADHD diagnosis in this age group compared to that currently recommended for younger ages. Findings were similar for parent-reports. Our findings suggest that the SDQ is suitable for ADHD research across different developmental periods, which will aid the robust investigation of ADHD from childhood to young adulthood. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
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