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Evaluation of the interaction between LRRK2 and PARK16 loci in determining risk of Parkinson's disease: analysis of a large multicenter study.

Lisa Wang, Michael G Heckman, Jan O Aasly, Grazia Annesi, Maria Bozi, Sun Ju Chung, Carl Clarke, David Crosiers, Gertrud Eckstein, Gaetan Garraux, Georgios M Hadjigeorgiou, Nobu Hattori, Beom Jeon, Yun J Kim, Masato Kubo, Suzanne Lesage, Juei Jueng Lin, Timothy Lynch, Peter Lichtner, George D Mellick, Vincent Mok, Karin E Morrison, Aldo Quattrone, Wataru Satake, Peter A Silburn, Leonidas Stefanis, Joanne D Stockton, Eng King Tan, Tatsushi Toda, Alexis Brice, Christine Van Broeckhoven, Ryan J Uitti, Karin Wirdefeldt, Zbigniew Wszolek, Georgia Xiromerisiou, Demetrius M Maraganore, Thomas Gasser, Rejko Krüger, Matthew J Farrer, Owen A Ross, Manu Sharma
Neurobiology of Aging 2017 January
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.

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