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Genome-wide analysis of copy number variants in attention deficit hyperactivity disorder

Williams, Nigel M. and Franke, Barbara and Mick, Eric and Anney, Richard J. L. and Freitag, Christine M. and Gill, Michael and Thapar, Anita and O'Donovan, Michael C. and Owen, Michael J. and Holmans, Peter and Kent, Lindsey and Middleton, Frank and Zhang-James, Yanli and Liu, Lu and Meyer, Jobst and Nguyen, Thuy Trang and Romanos, Jasmin and Romanos, Marcel and Seitz, Christiane and Renner, Tobias J. and Walitza, Susanne and Warnke, Andreas and Palmason, Haukur and Buitelaar, Jan and Rommelse, Nanda and Vasquez, Alejandro Arias and Hawi, Ziarih and Langley, Kate and Sergeant, Joseph and Steinhausen, Hans-Christoph and Roeyers, Herbert and Biederman, Joseph and Zaharieva, Irina and Hakonarson, Hakon and Elia, Josephine and Lionel, Anath C. and Crosbie, Jennifer and Marshall, Christian R. and Schachar, Russell and Scherer, Stephen W. and Todorov, Alexandre and Smalley, Susan L. and Loo, Sandra and Nelson, Stanley and Shtir, Corina and Asherson, Philip and Reif, Andreas and Lesch, Klaus-Peter and Faraone, Stephen V.. (2012) Genome-wide analysis of copy number variants in attention deficit hyperactivity disorder. American journal of psychiatry, Vol. 169, H. 2. pp. 195-204.

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Official URL: http://edoc.unibas.ch/dok/A6254496

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Abstract

Attention deficit hyperactivity disorder (ADHD) is a common, highly heritable psychiatric disorder. Because of its multifactorial etiology, however, identifying the genes involved has been difficult. The authors followed up on recent findings suggesting that rare copy number variants (CNVs) may be important for ADHD etiology.; The authors performed a genome-wide analysis of large, rare CNVs (>1% population frequency) in children with ADHD (N=896) and comparison subjects (N=2,455) from the IMAGE II Consortium.; The authors observed 1,562 individually rare CNVs <100 kb in size, which segregated into 912 independent loci. Overall, the rate of rare CNVs <100 kb was 1.15 times higher in ADHD case subjects relative to comparison subjects, with duplications spanning known genes showing a 1.2-fold enrichment. In accordance with a previous study, rare CNVs <500 kb showed the greatest enrichment (1.28-fold). CNVs identified in ADHD case subjects were significantly enriched for loci implicated in autism and in schizophrenia. Duplications spanning the CHRNA7 gene at chromosome 15q13.3 were associated with ADHD in single-locus analysis. This finding was consistently replicated in an additional 2,242 ADHD case subjects and 8,552 comparison subjects from four independent cohorts from the United Kingdom, the United States, and Canada. Presence of the duplication at 15q13.3 appeared to be associated with comorbid conduct disorder.; These findings support the enrichment of large, rare CNVs in ADHD and implicate duplications at 15q13.3 as a novel risk factor for ADHD. With a frequency of 0.6% in the populations investigated and a relatively large effect size (odds ratio=2.22, 95% confidence interval=1.5–3.6), this locus could be an important contributor to ADHD etiology.
Faculties and Departments:07 Faculty of Psychology > Departement Psychologie > Forschungsbereich Klinische Psychologie und Neurowissenschaften > Klinische Psychologie und Epidemiologie (Lieb)
UniBasel Contributors:Steinhausen, Hans-Christoph
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:American Psychiatric Association
ISSN:0002-953X
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:23 May 2014 08:34
Deposited On:23 May 2014 08:34

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