GeneSet Information

Tier I GS268202 • GWAS Catalog Data for attention deficit hyperactivity disorder in 495 European ancestry child and adolescent cases, 1,300 European ancestry adult controls

DESCRIPTION:

List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Attention deficit hyperactivity disorder. The EFO term attention deficit hyperactivity disorder was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.

LABEL:

GWAS: attention deficit hyperactivity disorder

SCORE TYPE:

P-Value

DATE ADDED:

2017-05-02

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

A Hinney, A Scherag, I Jarick, Ö Albayrak, C Pütter, S Pechlivanis, MR Dauvermann, S Beck, H Weber, S Scherag, TT Nguyen, AL Volckmar, N Knoll, SV Faraone, BM Neale, B Franke, S Cichon, P Hoffmann, MM Nöthen, S Schreiber, KH Jöckel, HE Wichmann, C Freitag, T Lempp, J Meyer, S Gilsbach, B Herpertz-Dahlmann, J Sinzig, G Lehmkuhl, TJ Renner, A Warnke, M Romanos, KP Lesch, A Reif, BG Schimmelmann, J Hebebrand

TITLE:

Genome-wide association study in German patients with attention deficit/hyperactivity disorder.

JOURNAL:

American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics Dec 2011, Vol 156B, pp. 888-97

ABSTRACT:

The heritability of attention deficit hyperactivity disorder (ADHD) is approximately 0.8. Despite several larger scale attempts, genome-wide association studies (GWAS) have not led to the identification of significant results. We performed a GWAS based on 495 German young patients with ADHD (according to DSM-IV criteria; Human660W-Quadv1; Illumina, San Diego, CA) and on 1,300 population-based adult controls (HumanHap550v3; Illumina). Some genes neighboring the single nucleotide polymorphisms (SNPs) with the lowest P-values (best P-value: 8.38 × 10(-7)) have potential relevance for ADHD (e.g., glutamate receptor, metabotropic 5 gene, GRM5). After quality control, the 30 independent SNPs with the lowest P-values (P-values ≤ 7.57 × 10(-5) ) were chosen for confirmation. Genotyping of these SNPs in up to 320 independent German families comprising at least one child with ADHD revealed directionally consistent effect-size point estimates for 19 (10 not consistent) of the SNPs. In silico analyses of the 30 SNPs in the largest meta-analysis so far (2,064 trios, 896 cases, and 2,455 controls) revealed directionally consistent effect-size point estimates for 16 SNPs (11 not consistent). None of the combined analyses revealed a genome-wide significant result. SNPs in previously described autosomal candidate genes did not show significantly lower P-values compared to SNPs within random sets of genes of the same size. We did not find genome-wide significant results in a GWAS of German children with ADHD compared to controls. The second best SNP is located in an intron of GRM5, a gene located within a recently described region with an infrequent copy number variation in patients with ADHD. PUBMED: 22012869
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attention deficit hyperactivity disorder (EFO:0003888)

Gene List • 2 Genes

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