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Study Report - GWAS of Parkinson's disease (HGVST6)| HGVbaseG2P identifier | HGVST6 | |||||||||||||||
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| Study name | GWAS of Parkinson's disease | |||||||||||||||
| Phenotype(s) tested | Parkinson's disease |
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| Study design | Case and control | |||||||||||||||
| Genotype Platforms |
Illumina HumanHap300 Illumina Infinium I | |||||||||||||||
| Abstract | Summary-level data and analysis results from the National Institute of Neurological Disorders and Stroke (NINDS) Parkinson's disease project imported from dbGaP. BACKGROUND: Several genes underlying rare monogenic forms of Parkinson's disease have been identified over the past decade. Despite evidence for a role for genetics in sporadic Parkinson's disease, few common genetic variants have been unequivocally linked to this disorder. We sought to identify any common genetic variability exerting a large effect in risk for Parkinson's disease in a population cohort and to produce publicly available genome-wide genotype data that can be openly mined by interested researchers and readily augmented by genotyping of additional repository subjects. METHODS: We did genome-wide, single-nucleotide-polymorphism (SNP) genotyping of publicly available samples from a cohort of Parkinson's disease patients (n=267) and neurologically normal controls (n=270). More than 408,000 unique SNPs were used from the Illumina Infinium I and HumanHap300 assays. FINDINGS: We have produced around 220 million genotypes in 537 participants. This raw genotype data has been and as such is the first publicly accessible high-density SNP data outside of the International HapMap Project. We also provide here the results of genotype and allele association tests. INTERPRETATION: We generated publicly available genotype data for Parkinson's disease patients and controls so that these data can be mined and augmented by other researchers to identify common genetic variability that results in minor and moderate risk for disease. | |||||||||||||||
| Submission information |
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| Cross-references |
dbGaP - NINDS Parkinson's |
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| Background | Not supplied | |||||||||||||||
| Objectives | Not supplied | |||||||||||||||
| Key results | Not supplied | |||||||||||||||
| Conclusions | Not supplied | |||||||||||||||
| Reason for study size | Not supplied | |||||||||||||||
| Study power | Not supplied | |||||||||||||||
| Sources of bias | Not supplied | |||||||||||||||
| Limitations | Not supplied | |||||||||||||||
| Acknowledgements | Not supplied | |||||||||||||||
| Other citations |
Fung HC, Scholz S, Matarin M et al.
Genome-wide genotyping in Parkinson's disease and neurologically normal controls:first stage analysis and public release of data Lancet Neurol 2006 Nov;5(11):911-6
Simon-Sanchez J, Scholz S, Fung HC et al.
Genome-wide SNP assay reveals structural genomic variation, extended homozygosity and cell-line induced alterations in normal individuals Hum Mol Genet 2007 Jan 1;16(1):1-14 |
