[en] 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.
Disciplines :
Neurology
Author, co-author :
Wang, Lisa
Heckman, Michael G.
Aasly, Jan O.
Annesi, Grazia
Bozi, Maria
Chung, Sun Ju
Clarke, Carl
Crosiers, David
Eckstein, Gertrud
Garraux, Gaetan
Hadjigeorgiou, Georgios M.
Hattori, Nobu
Jeon, Beom
Kim, Yun J.
Kubo, Masato
Lesage, Suzanne
Lin, Juei Jueng
Lynch, Timothy
Lichtner, Peter
Mellick, George D.
Mok, Vincent
Morrison, Karin E.
Quattrone, Aldo
Satake, Wataru
Silburn, Peter A.
Stefanis, Leonidas
Stockton, Joanne D.
Tan, Eng King
Toda, Tatsushi
Brice, Alexis
Van Broeckhoven, Christine
Uitti, Ryan J.
Wirdefeldt, Karin
Wszolek, Zbigniew
Xiromerisiou, Georgia
Maraganore, Demetrius M.
Gasser, Thomas
Krüger, Rejko ; University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit
