| Literature DB >> 24842889 |
Vladimir Vacic1, Laurie J Ozelius2, Lorraine N Clark3, Anat Bar-Shira4, Mali Gana-Weisz4, Tanya Gurevich5, Alexander Gusev1, Merav Kedmi4, Eimear E Kenny1, Xinmin Liu6, Helen Mejia-Santana7, Anat Mirelman8, Deborah Raymond9, Rachel Saunders-Pullman10, Robert J Desnick11, Gil Atzmon12, Edward R Burns13, Harry Ostrer14, Hakon Hakonarson15, Aviv Bergman16, Nir Barzilai12, Ariel Darvasi17, Inga Peter11, Saurav Guha18, Todd Lencz19, Nir Giladi5, Karen Marder20, Itsik Pe'er21, Susan B Bressman10, Avi Orr-Urtreger22.
Abstract
The recent series of large genome-wide association studies in European and Japanese cohorts established that Parkinson disease (PD) has a substantial genetic component. To further investigate the genetic landscape of PD, we performed a genome-wide scan in the largest to date Ashkenazi Jewish cohort of 1130 Parkinson patients and 2611 pooled controls. Motivated by the reduced disease allele heterogeneity and a high degree of identical-by-descent (IBD) haplotype sharing in this founder population, we conducted a haplotype association study based on mapping of shared IBD segments. We observed significant haplotype association signals at three previously implicated Parkinson loci: LRRK2 (OR = 12.05, P = 1.23 × 10(-56)), MAPT (OR = 0.62, P = 1.78 × 10(-11)) and GBA (multiple distinct haplotypes, OR > 8.28, P = 1.13 × 10(-11) and OR = 2.50, P = 1.22 × 10(-9)). In addition, we identified a novel association signal on chr2q14.3 coming from a rare haplotype (OR = 22.58, P = 1.21 × 10(-10)) and replicated it in a secondary cohort of 306 Ashkenazi PD cases and 2583 controls. Our results highlight the power of our haplotype association method, particularly useful in studies of founder populations, and reaffirm the benefits of studying complex diseases in Ashkenazi Jewish cohorts.Entities:
Mesh:
Year: 2014 PMID: 24842889 PMCID: PMC4119402 DOI: 10.1093/hmg/ddu158
Source DB: PubMed Journal: Hum Mol Genet ISSN: 0964-6906 Impact factor: 6.150