Journal
NATURE GENETICS
Volume 41, Issue 12, Pages 1308-U68Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.487
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Funding
- Intramural Research Programs of the National Institute on Aging
- National Institute of Neurological Disorders and Stroke
- National Institute of Environmental Health Sciences
- National Cancer Institute
- National Institutes of Health
- Department of Health and Human Services [Z01 AG000949-02, Z01-ES101986]
- Forschungszentrum fur Umwelt und Gesundheit (GSF)
- German Federal Ministry of Education, Science, Research and Technology
- State of Bavaria
- German National Genome Network [01GS08134]
- German Ministry for Education and Research
- German Federal Ministry of Education and Research (BMBF) NGFN [01GR0468]
- National Institutes of Health NINDS [P30NS05710]
- Clinical Sciences Translational Award [RR024992]
- Medical Research Council, UK
- Medical Research Council [G0400000, G0701075, G108/638] Funding Source: researchfish
- Parkinson's UK [G-0907, J-0804, G-0909] Funding Source: researchfish
- MRC [G0400000, G0701075, G108/638] Funding Source: UKRI
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We performed a genome-wide association study (GWAS) in 1,713 individuals of European ancestry with Parkinson's disease (PD) and 3,978 controls. After replication in 3,361 cases and 4,573 controls, we observed two strong association signals, one in the gene encoding a-synuclein (SNCA; rs2736990, OR = 1.23, P = 2.24 x 10(-16)) and another at the MAPT locus (rs393152, OR = 0.77, P = 1.95 x 10(-16)). We exchanged data with colleagues performing a GWAS in Japanese PD cases. Association to PD at SNCA was replicated in the Japanese GWAS1, confirming this as a major risk locus across populations. We replicated the effect of a new locus detected in the Japanese cohort (PARK16, rs823128, OR = 0.66, P = 7.29 x 10(-8)) and provide supporting evidence that common variation around LRRK2 modulates risk for PD (rs1491923, OR = 1.14, P = 1.55 x 10(-5)). These data demonstrate an unequivocal role for common genetic variants in the etiology of typical PD and suggest population-specific genetic heterogeneity in this disease.
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