Polygenic transmission and complex neuro developmental network for attention deficit hyperactivity disorder: genome-wide association study of both common and rare variants.
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Authors
Yang, LiNeale, Benjamin M
Liu, Lu
Lee, S Hong
Wray, Naomi R
Ji, Ning
Li, Haimei
Qian, Qiujin
Wang, Dongliang
Li, Jun
Faraone, Stephen V
Wang, Yufeng
Doyle, Alysa E
Reif, Andreas
Rothenberger, Aribert
Franke, Barbara
Sonuga-Barke, Edmund J S
Steinhausen, Hans-Christoph
Buitelaar, Jan K
Kuntsi, Jonna
Biederman, Joseph
Lesch, Klaus-Peter
Kent, Lindsey
Asherson, Philip
Oades, Robert D
Loo, Sandra K
Nelson, Stan F
Faraone, Stephen V
Smalley, Susan L
Banaschewski, Tobias
Arias Vasquez, Alejandro
Todorov, Alexandre
Charach, Alice
Miranda, Ana
Warnke, Andreas
Thapar, Anita
Neale, Benjamin M
Cormand, Bru
Freitag, Christine
Mick, Eric
Mulas, Fernando
Middleton, Frank
HakonarsonHakonarson, Hakon
Palmason, Haukur
Schäfer, Helmut
Roeyers, Herbert
McGough, James J
Romanos, Jasmin
Crosbie, Jennifer
Meyer, Jobst
Ramos-Quiroga, Josep Antoni
Sergeant, Joseph
Elia, Josephine
Langely, Kate
Nisenbaum, Laura
Romanos, Marcel
Daly, Mark J
Ribasés, Marta
Gill, Michael
O'Donovan, Michael
Owen, Michael
Casas, Miguel
Bayés, Mònica
Lambregts-Rommelse, Nanda
Williams, Nigel
Holmans, Peter
Anney, Richard J L
Ebstein, Richard P
Schachar, Russell
Medland, Sarah E
Ripke, Stephan
Walitza, Susanne
Nguyen, Thuy Trang
Renner, Tobias J
Hu, Xiaolan
Issue Date
2013-07
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Am. J. Med. Genet. B Neuropsychiatr. Genet. 2013, 162B (5):419-30Abstract
Attention-deficit hyperactivity disorder (ADHD) is a complex polygenic disorder. This study aimed to discover common and rare DNA variants associated with ADHD in a large homogeneous Han Chinese ADHD case-control sample. The sample comprised 1,040 cases and 963 controls. All cases met DSM-IV ADHD diagnostic criteria. We used the Affymetrix6.0 array to assay both single nucleotide polymorphisms (SNPs) and copy number variants (CNVs). Genome-wide association analyses were performed using PLINK. SNP-heritability and SNP-genetic correlations with ADHD in Caucasians were estimated with genome-wide complex trait analysis (GCTA). Pathway analyses were performed using the Interval enRICHment Test (INRICH), the Disease Association Protein-Protein Link Evaluator (DAPPLE), and the Genomic Regions Enrichment of Annotations Tool (GREAT). We did not find genome-wide significance for single SNPs but did find an increased burden of large, rare CNVs in the ADHD sample (P = 0.038). SNP-heritability was estimated to be 0.42 (standard error, 0.13, P = 0.0017) and the SNP-genetic correlation with European Ancestry ADHD samples was 0.39 (SE 0.15, P = 0.0072). The INRICH, DAPPLE, and GREAT analyses implicated several gene ontology cellular components, including neuron projections and synaptic components, which are consistent with a neurodevelopmental pathophysiology for ADHD. This study suggested the genetic architecture of ADHD comprises both common and rare variants. Some common causal variants are likely to be shared between Han Chinese and Caucasians. Complex neurodevelopmental networks may underlie ADHD's etiology.Description
To access publisher's full text version of this article click on the hyperlink at the bottom of the pageAdditional Links
http://dx.doi.org/10.1002/ajmg.b.32169http://adhdnet.com/wp/wp-content/uploads/2013/01/Yang-2013-Polygenic-transmission-and-co.pdf
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Archived with thanks to American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Geneticsae974a485f413a2113503eed53cd6c53
10.1002/ajmg.b.32169
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