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author Simon-Sanchez, Javier
Schulte, Claudia
Bras, Jose M
Sharma, Manu
Gibbs, J Raphael
Berg, Daniela
Paisan-Ruiz, Coro
Lichtner, Peter
Scholz, Sonja W
Hernandez, Dena G
Kruger, Rejko
Federoff, Monica
Klein, Christine
Goate, Alison
Perlmutter, Joel
Bonin, Michael
Nalls, Michael A
Illig, Thomas
Gieger, Christian
Houlden, Henry
Steffens, Michael
Okun, Michael S.
Cookson, Mark
Foote, Kelly D
Fernandez, Hubert H
Traynor, Bryan J.
Schreiber, Stefan
Arepalli, Sampath
Zonozi, Ryan
Gwinn, Katrina
van der Brug, Marcel
Lopez, Grisel
Chanock, Stephen J
Schatzkin, Arthur
Park, Yikyung
Hollenbeck, Albert
Gao, Jianjun
Huang, Xuemei
Wood, Nick W
Lorenz, Delia
Deuschl, Gunther
Chen, Honglei
Riess, Olaf
Hardy, John A
Singleton, Andrew B
Gasser, Thomas
author_facet Simon-Sanchez, Javier
Schulte, Claudia
Bras, Jose M
Sharma, Manu
Gibbs, J Raphael
Berg, Daniela
Paisan-Ruiz, Coro
Lichtner, Peter
Scholz, Sonja W
Hernandez, Dena G
Kruger, Rejko
Federoff, Monica
Klein, Christine
Goate, Alison
Perlmutter, Joel
Bonin, Michael
Nalls, Michael A
Illig, Thomas
Gieger, Christian
Houlden, Henry
Steffens, Michael
Okun, Michael S.
Cookson, Mark
Foote, Kelly D
Fernandez, Hubert H
Traynor, Bryan J.
Schreiber, Stefan
Arepalli, Sampath
Zonozi, Ryan
Gwinn, Katrina
van der Brug, Marcel
Lopez, Grisel
Chanock, Stephen J
Schatzkin, Arthur
Park, Yikyung
Hollenbeck, Albert
Gao, Jianjun
Huang, Xuemei
Wood, Nick W
Lorenz, Delia
Deuschl, Gunther
Chen, Honglei
Riess, Olaf
Hardy, John A
Singleton, Andrew B
Gasser, Thomas
author_sort Simon-Sanchez, Javier
collection PubMed
description We performed a genome-wide association study (GWAS) in 1,713 Caucasian patients with Parkinson’s disease (PD) and 3,978 controls. After replication in 3,361 cases and 4,573 controls, two strong association signals were observed: in the α-synuclein gene(SNCA) (rs2736990, OR=1.23, p=2.24×10(−16)) and at the MAPT locus (rs393152, OR=0.77, p=1.95×10(−16)). We exchanged data with colleagues performing a GWAS in Asian PD cases. Association at SNCA was replicated in the Asian GWAS1, confirming this as a major risk locus across populations. We were able to replicate the effect of a novel locus detected in the Asian cohort (PARK16, rs823128, OR=0.66, p=7.29×10(−8)) and provide evidence supporting the role of common variability around LRRK2 in modulating risk for PD (rs1491923, OR=1.14, p=1.55×10(−5)). These data demonstrate an unequivocal role for common genetic variability in the etiology of typical PD and suggest population specific genetic heterogeneity in this disease.
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spelling pubmed-27877252010-06-01 Genome-Wide Association Study reveals genetic risk underlying Parkinson’s disease Simon-Sanchez, Javier Schulte, Claudia Bras, Jose M Sharma, Manu Gibbs, J Raphael Berg, Daniela Paisan-Ruiz, Coro Lichtner, Peter Scholz, Sonja W Hernandez, Dena G Kruger, Rejko Federoff, Monica Klein, Christine Goate, Alison Perlmutter, Joel Bonin, Michael Nalls, Michael A Illig, Thomas Gieger, Christian Houlden, Henry Steffens, Michael Okun, Michael S. Cookson, Mark Foote, Kelly D Fernandez, Hubert H Traynor, Bryan J. Schreiber, Stefan Arepalli, Sampath Zonozi, Ryan Gwinn, Katrina van der Brug, Marcel Lopez, Grisel Chanock, Stephen J Schatzkin, Arthur Park, Yikyung Hollenbeck, Albert Gao, Jianjun Huang, Xuemei Wood, Nick W Lorenz, Delia Deuschl, Gunther Chen, Honglei Riess, Olaf Hardy, John A Singleton, Andrew B Gasser, Thomas Nat Genet Article We performed a genome-wide association study (GWAS) in 1,713 Caucasian patients with Parkinson’s disease (PD) and 3,978 controls. After replication in 3,361 cases and 4,573 controls, two strong association signals were observed: in the α-synuclein gene(SNCA) (rs2736990, OR=1.23, p=2.24×10(−16)) and at the MAPT locus (rs393152, OR=0.77, p=1.95×10(−16)). We exchanged data with colleagues performing a GWAS in Asian PD cases. Association at SNCA was replicated in the Asian GWAS1, confirming this as a major risk locus across populations. We were able to replicate the effect of a novel locus detected in the Asian cohort (PARK16, rs823128, OR=0.66, p=7.29×10(−8)) and provide evidence supporting the role of common variability around LRRK2 in modulating risk for PD (rs1491923, OR=1.14, p=1.55×10(−5)). These data demonstrate an unequivocal role for common genetic variability in the etiology of typical PD and suggest population specific genetic heterogeneity in this disease. 2009-11-15 2009-12 /pmc/articles/PMC2787725/ /pubmed/19915575 http://dx.doi.org/10.1038/ng.487 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Simon-Sanchez, Javier
Schulte, Claudia
Bras, Jose M
Sharma, Manu
Gibbs, J Raphael
Berg, Daniela
Paisan-Ruiz, Coro
Lichtner, Peter
Scholz, Sonja W
Hernandez, Dena G
Kruger, Rejko
Federoff, Monica
Klein, Christine
Goate, Alison
Perlmutter, Joel
Bonin, Michael
Nalls, Michael A
Illig, Thomas
Gieger, Christian
Houlden, Henry
Steffens, Michael
Okun, Michael S.
Cookson, Mark
Foote, Kelly D
Fernandez, Hubert H
Traynor, Bryan J.
Schreiber, Stefan
Arepalli, Sampath
Zonozi, Ryan
Gwinn, Katrina
van der Brug, Marcel
Lopez, Grisel
Chanock, Stephen J
Schatzkin, Arthur
Park, Yikyung
Hollenbeck, Albert
Gao, Jianjun
Huang, Xuemei
Wood, Nick W
Lorenz, Delia
Deuschl, Gunther
Chen, Honglei
Riess, Olaf
Hardy, John A
Singleton, Andrew B
Gasser, Thomas
Genome-Wide Association Study reveals genetic risk underlying Parkinson’s disease
title Genome-Wide Association Study reveals genetic risk underlying Parkinson’s disease
title_full Genome-Wide Association Study reveals genetic risk underlying Parkinson’s disease
title_fullStr Genome-Wide Association Study reveals genetic risk underlying Parkinson’s disease
title_full_unstemmed Genome-Wide Association Study reveals genetic risk underlying Parkinson’s disease
title_short Genome-Wide Association Study reveals genetic risk underlying Parkinson’s disease
title_sort genome-wide association study reveals genetic risk underlying parkinson’s disease
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2787725/
https://www.ncbi.nlm.nih.gov/pubmed/19915575
http://dx.doi.org/10.1038/ng.487
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