Separation of cognitive impairments in attention-deficit/hyperactivity disorder into 2 familial factors

Attention-deficit/hyperactivity disorder (ADHD) is associated with widespread cognitive impairments, but it is not known whether the apparent multiple impairments share etiological roots or separate etiological pathways exist. A better understanding of the etiological pathways is important for the d...

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Hauptverfasser: Kuntsi, Jonna (VerfasserIn) , Wood, Alexis C. (VerfasserIn) , Johnson, Katherine A. (VerfasserIn) , Andreou, Penelope (VerfasserIn) , Arias-Vasquez, Alejandro (VerfasserIn) , Buitelaar, Jan K. (VerfasserIn) , Rommelse, Nanda N. J. (VerfasserIn) , Sergeant, Joseph A. (VerfasserIn) , Sonuga-Barke, Edmund J. (VerfasserIn) , Uebel, Henrik (VerfasserIn) , van der Meere, Jaap J. (VerfasserIn) , Banaschewski, Tobias (VerfasserIn) , Gill, Michael (VerfasserIn) , Manor, Iris (VerfasserIn) , Miranda, Ana (VerfasserIn) , Mulas, Fernando (VerfasserIn) , Oades, Robert D. (VerfasserIn) , Roeyers, Herbert (VerfasserIn) , Rothenberger, Aribert (VerfasserIn) , Steinhausen, Hans-Christoph (VerfasserIn) , Faraone, Stephen V. (VerfasserIn) , Asherson, Philip (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: November 2010
In: Archives of general psychiatry
Year: 2010, Jahrgang: 67, Heft: 11, Pages: 1159-1166
ISSN:1538-3636
DOI:10.1001/archgenpsychiatry.2010.139
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1001/archgenpsychiatry.2010.139
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Verfasserangaben:Jonna Kuntsi, Alexis C. Wood, Katherine A. Johnson, Penelope Andreou, Alejandro Arias-Vasquez, Jan K. Buitelaar, Nanda N.J. Rommelse, Joseph A. Sergeant, Edmund J. Sonuga-Barke, Henrik Uebel, Jaap J. van der Meere, Tobias Banaschewski, Michael Gill, Iris Manor, Ana Miranda, Fernando Mulas, Robert D. Oades, Herbert Roeyers, Aribert Rothenberger, Hans-Christoph Steinhausen, Stephen V. Faraone, Philip Asherson
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Zusammenfassung:Attention-deficit/hyperactivity disorder (ADHD) is associated with widespread cognitive impairments, but it is not known whether the apparent multiple impairments share etiological roots or separate etiological pathways exist. A better understanding of the etiological pathways is important for the development of targeted interventions and for identification of suitable intermediate phenotypes for molecular genetic investigations.To determine, by using a multivariate familial factor analysis approach, whether 1 or more familial factors underlie the slow and variable reaction times, impaired response inhibition, and choice impulsivity associated with ADHD.An ADHD and control sibling-pair design.Belgium, Germany, Ireland, Israel, Spain, Switzerland, and the United Kingdom.A total of 1265 participants, aged 6 to 18 years: 464 probands with ADHD and 456 of their siblings (524 with combined-subtype ADHD), and 345 control participants.Performance on a 4-choice reaction time task, a go/no-go inhibition task, and a choice-delay task.The final model consisted of 2 familial factors. The larger factor, reflecting 85% of the familial variance of ADHD, captured 98% to 100% of the familial influences on mean reaction time and reaction time variability. The second, smaller factor, reflecting 13% of the familial variance of ADHD, captured 62% to 82% of the familial influences on commission and omission errors on the go/no-go task. Choice impulsivity was excluded in the final model because of poor fit.The findings suggest the existence of 2 familial pathways to cognitive impairments in ADHD and indicate promising cognitive targets for future molecular genetic investigations. The familial distinction between the 2 cognitive impairments is consistent with recent theoretical models—a developmental model and an arousal-attention model—of 2 separable underlying processes in ADHD. Future research that tests the familial model within a developmental framework may inform developmentally sensitive interventions.Arch Gen Psychiatry. 2010;67(11):1159-1167-->
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Beschreibung:Online Resource
ISSN:1538-3636
DOI:10.1001/archgenpsychiatry.2010.139