Literaturnachweis - Detailanzeige
Autor/inn/en | Mick, Eric; Todorov, Alexandre; Smalley, Susan; Hu, Xiaolan; Loo, Sandra; Todd, Richard D.; Biederman, Joseph; Byrne, Deirdre; Dechairo, Bryan; Guiney, Allan; McCracken, James; McGough, James; Nelson, Stanley F.; Reiersen, Angela M.; Wilens, Timothy E.; Wozniak, Janet; Neale, Benjamin M.; Faraone, Stephen V. |
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Titel | Family-Based Genome-Wide Association Scan of Attention-Deficit/Hyperactivity Disorder |
Quelle | In: Journal of the American Academy of Child & Adolescent Psychiatry, 49 (2010) 9, S.898-905 (8 Seiten)
PDF als Volltext |
Sprache | englisch |
Dokumenttyp | gedruckt; online; Zeitschriftenaufsatz |
ISSN | 0890-8567 |
DOI | 10.1016/j.jaac.2010.02.014 |
Schlagwörter | Evidence; Attention Deficit Hyperactivity Disorder; Quality Control; Genetics; Statistical Significance; Etiology; Identification; Family Involvement; Research Methodology; Science Education; Biology; California; Massachusetts; Missouri |
Abstract | Objective: Genes likely play a substantial role in the etiology of attention-deficit/hyperactivity disorder (ADHD). However, the genetic architecture of the disorder is unknown, and prior genome-wide association studies (GWAS) have not identified a genome-wide significant association. We have conducted a third, independent, multisite GWAS of DSM-IV-TR ADHD. Method: Families were ascertained at Massachusetts General Hospital (MGH; N = 309 trios), Washington University at St. Louis (WASH-U; N = 272 trios), and University of California at Los Angeles (UCLA; N = 156 trios). Genotyping was conducted with the Illumina Human1M or Human1M-Duo BeadChip platforms. After applying quality control filters, association with ADHD was tested with 835,136 SNPs in 735 DSM-IV ADHD trios from 732 families. Results: Our smallest p value (6.7E-07) did not reach the threshold for genome-wide statistical significance (5.0E-08), but one of the 20 most significant associations was located in a candidate gene of interest for ADHD (SLC9A9, rs9810857, p = 6.4E-6). We also conducted gene-based tests of candidate genes identified in the literature and found additional evidence of association with SLC9A9. Conclusions: We and our colleagues in the Psychiatric GWAS Consortium are working to pool together GWAS samples to establish the large data sets needed to follow-up on these results and to identify genes for ADHD and other disorders. (Contains 3 figures and 5 tables.) (As Provided). |
Anmerkungen | Elsevier. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. Tel: 877-839-7126; Tel: 407-345-4020; Fax: 407-363-1354; e-mail: usjcs@elsevier.com; Web site: http://www.elsevier.com |
Erfasst von | ERIC (Education Resources Information Center), Washington, DC |
Update | 2017/4/10 |