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. MellickVincent Mok, Karin 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

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)

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
Original languageEnglish
Pages (from-to)217.e1-217.e4
Number of pages4
JournalNeurobiology of Aging
Volume49
Early online date06 Oct 2016
DOIs
Publication statusPublished - Jan 2017
Externally publishedYes

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