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Genome-wide association scan of attention deficit hyperactivity disorder (In special issue: Special Issue on the Genetics of ADHD Dedicated to the Memory of Richard Todd)

Genome-wide association scan of attention deficit hyperactivity disorder (In special issue: Special Issue on the Genetics of ADHD Dedicated to the Memory of Richard Todd)
Genome-wide association scan of attention deficit hyperactivity disorder (In special issue: Special Issue on the Genetics of ADHD Dedicated to the Memory of Richard Todd)
Results of behavioral genetic and molecular genetic studies have converged to suggest that genes substantially contribute to the development of attention deficit/hyperactivity disorder (ADHD), a common disorder with an onset in childhood. Yet, despite numerous linkage and candidate gene studies, strongly consistent and replicable association has eluded detection. To search for ADHD susceptibility genes, we genotyped approximately 600,000 SNPs in 958 ADHD affected family trios. After cleaning the data, we analyzed 438,784 SNPs in 2,803 individuals comprising 909 complete trios using ADHD diagnosis as phenotype. We present the initial TDT findings as well as considerations for cleaning family-based TDT data. None of the SNP association tests achieved genome-wide significance, indicating that larger samples may be required to identify risk loci for ADHD. We additionally identify a systemic bias in family-based association, and suggest that variable missing genotype rates may be the source of this bias.
1552-4841
1337-1344
Neale, Benjamin M.
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Lasky-Su, Jessica
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Anney, Richard
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Franke, Barbara
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Zhou, Kaixin
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Maller, Julian B.
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Arias-Vasquez, Alejandro
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Asherson, Philip
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Chen, Wai
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Banaschewski, Tobias
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Buitelaar, Jan
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Ebstein, Richard
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Gill, Michael
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Miranda, Ana
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Oades, Robert D.
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Roeyers, Herbert
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Rothenberger, Aribert
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Sergeant, Joseph
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Steinhausen, Hans Christoph
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Sonuga-Barke, Edmund
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Mulas, Fernando
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Taylor, Eric
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Laird, Nan
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Lange, Christoph
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Daly, Mark
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Faraone, Stephen V.
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Neale, Benjamin M.
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Lasky-Su, Jessica
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Anney, Richard
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Franke, Barbara
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Zhou, Kaixin
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Maller, Julian B.
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Arias-Vasquez, Alejandro
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Asherson, Philip
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Chen, Wai
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Banaschewski, Tobias
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Buitelaar, Jan
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Ebstein, Richard
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Gill, Michael
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Miranda, Ana
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Oades, Robert D.
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Roeyers, Herbert
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Rothenberger, Aribert
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Sergeant, Joseph
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Steinhausen, Hans Christoph
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Sonuga-Barke, Edmund
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Mulas, Fernando
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Taylor, Eric
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Laird, Nan
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Lange, Christoph
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Daly, Mark
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Faraone, Stephen V.
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Neale, Benjamin M., Lasky-Su, Jessica, Anney, Richard, Franke, Barbara, Zhou, Kaixin, Maller, Julian B., Arias-Vasquez, Alejandro, Asherson, Philip, Chen, Wai, Banaschewski, Tobias, Buitelaar, Jan, Ebstein, Richard, Gill, Michael, Miranda, Ana, Oades, Robert D., Roeyers, Herbert, Rothenberger, Aribert, Sergeant, Joseph, Steinhausen, Hans Christoph, Sonuga-Barke, Edmund, Mulas, Fernando, Taylor, Eric, Laird, Nan, Lange, Christoph, Daly, Mark and Faraone, Stephen V. (2008) Genome-wide association scan of attention deficit hyperactivity disorder (In special issue: Special Issue on the Genetics of ADHD Dedicated to the Memory of Richard Todd). American Journal of Medical Genetics. Part B: Neuropsychiatric Genetics, 147B (8), 1337-1344. (doi:10.1002/ajmg.b.30866).

Record type: Article

Abstract

Results of behavioral genetic and molecular genetic studies have converged to suggest that genes substantially contribute to the development of attention deficit/hyperactivity disorder (ADHD), a common disorder with an onset in childhood. Yet, despite numerous linkage and candidate gene studies, strongly consistent and replicable association has eluded detection. To search for ADHD susceptibility genes, we genotyped approximately 600,000 SNPs in 958 ADHD affected family trios. After cleaning the data, we analyzed 438,784 SNPs in 2,803 individuals comprising 909 complete trios using ADHD diagnosis as phenotype. We present the initial TDT findings as well as considerations for cleaning family-based TDT data. None of the SNP association tests achieved genome-wide significance, indicating that larger samples may be required to identify risk loci for ADHD. We additionally identify a systemic bias in family-based association, and suggest that variable missing genotype rates may be the source of this bias.

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Published date: 5 December 2008

Identifiers

Local EPrints ID: 64137
URI: http://eprints.soton.ac.uk/id/eprint/64137
ISSN: 1552-4841
PURE UUID: 6b8fb502-7b72-4575-a751-a56eadd1dff7

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Date deposited: 04 Dec 2008
Last modified: 15 Mar 2024 11:46

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Contributors

Author: Benjamin M. Neale
Author: Jessica Lasky-Su
Author: Richard Anney
Author: Barbara Franke
Author: Kaixin Zhou
Author: Julian B. Maller
Author: Alejandro Arias-Vasquez
Author: Philip Asherson
Author: Wai Chen
Author: Tobias Banaschewski
Author: Jan Buitelaar
Author: Richard Ebstein
Author: Michael Gill
Author: Ana Miranda
Author: Robert D. Oades
Author: Herbert Roeyers
Author: Aribert Rothenberger
Author: Joseph Sergeant
Author: Hans Christoph Steinhausen
Author: Edmund Sonuga-Barke
Author: Fernando Mulas
Author: Eric Taylor
Author: Nan Laird
Author: Christoph Lange
Author: Mark Daly
Author: Stephen V. Faraone

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