Evaluation of the interaction between LRRK2 and PARK16 loci in determining risk of Parkinson’s disease: analysis of a large multi-center study

Publication date: Available online 6 October 2016
Source:Neurobiology of Aging
Author(s): L. Wang, M.G. Heckman, J.O. Aasly, G. Annesi, M. Bozi, S.J. Chung, C. Clarke, D. Crosiers, G. Eckstein, G. Garraux, G.M. Hadjigeorgiou, N. Hattori, B. Jeon, Y.J. Kim, M. Kubo, S. Lesage, J.J. Lin, T. Lynch, P. Lichtner, G.D. Mellick, V. Mok, K.E. Morrison, A. Quattrone, W. Satake, P.A. Silburn, L. Stefanis, J.D. Stockton, E.K. Tan, T. Toda, A. Brice, C. Van Broeckhoven, R.J. Uitti, K. Wirdefeldt, Z. Wszolek, G. Xiromerisiou, D.M. Maraganore, T. Gasser, R. Krüger, M.J. Farrer, O.A. Ross, M. Sharma
A recent study has shown that an interaction between variants at the LRRK2 and PARK16 loci influences risk of development of PD (MacLeod D. et al, 2013). Our study examines the proposed interaction between LRRK2 and PARK16 variants in modifying PD risk using a large multi-center series of PD patients (5769) and controls (4988) from sites participating in the Genetic Epidemiology of Parkinson's Disease (GEoPD) 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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