| Literature DB >> 27814993 |
Lisa Wang1, Michael G Heckman2, Jan O Aasly3, Grazia Annesi4, Maria Bozi5, Sun Ju Chung6, Carl Clarke7, David Crosiers8, Gertrud Eckstein9, Gaetan Garraux10, Georgios M Hadjigeorgiou11, Nobu Hattori12, Beom Jeon13, Yun J Kim14, Masato Kubo15, Suzanne Lesage16, Juei Jueng Lin17, Timothy Lynch18, Peter Lichtner9, George D Mellick19, Vincent Mok20, Karin E Morrison21, Aldo Quattrone22, Wataru Satake23, Peter A Silburn24, Leonidas Stefanis25, Joanne D Stockton26, Eng King Tan27, Tatsushi Toda23, Alexis Brice16, Christine Van Broeckhoven28, Ryan J Uitti29, Karin Wirdefeldt30, Zbigniew Wszolek29, Georgia Xiromerisiou11, Demetrius M Maraganore31, Thomas Gasser32, Rejko Krüger33, Matthew J Farrer34, Owen A Ross35, Manu Sharma36.
Abstract
A recent study MacLeod et al. has shown that an interaction between variants at the LRRK2 and PARK16 loci influences risk of development of Parkinson's disease (PD). Our study examines the proposed interaction between LRRK2 and PARK16 variants in modifying PD risk using a large multicenter series of PD patients (7715) and controls (8261) from sites participating in the Genetic Epidemiology of Parkinson's Disease Consortium. Our data does not support a strong direct interaction between LRRK2 and PARK16 variants; however, given the role of retromer and lysosomal pathways in PD, further studies are warranted.Entities:
Keywords: Genetic epidemiology; LRRK2; PARK16; Parkinson's disease
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Year: 2016 PMID: 27814993 PMCID: PMC5154911 DOI: 10.1016/j.neurobiolaging.2016.09.022
Source DB: PubMed Journal: Neurobiol Aging ISSN: 0197-4580 Impact factor: 4.673