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

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

doi:10.1016/j.neurobiolaging.2016.09.022

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.

Full Text