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

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 seri...

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Veröffentlicht in:Neurobiology of aging 2017-01, Vol.49, p.217.e1-217.e4
Hauptverfasser: 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, Farrer, Matthew J., Ross, Owen A., Sharma, Manu
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container_issue
container_start_page 217.e1
container_title Neurobiology of aging
container_volume 49
creator 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
Farrer, Matthew J.
Ross, Owen A.
Sharma, Manu
description 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.
doi_str_mv 10.1016/j.neurobiolaging.2016.09.022
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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.</description><subject>Epistasis, Genetic</subject><subject>Epistasis, Genetic - genetics</subject><subject>Genetic Association Studies</subject><subject>Genetic epidemiology</subject><subject>Genetic Loci</subject><subject>Genetic Loci - genetics</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genetic Variation</subject><subject>Genetic Variation - genetics</subject><subject>Human health and pathology</subject><subject>Humans</subject><subject>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</subject><subject>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 - genetics</subject><subject>Life Sciences</subject><subject>LRRK2</subject><subject>Multicenter Studies as Topic</subject><subject>PARK16</subject><subject>Parkinson Disease</subject><subject>Parkinson Disease - 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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.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>27814993</pmid><doi>10.1016/j.neurobiolaging.2016.09.022</doi><orcidid>https://orcid.org/0000-0002-0941-3990</orcidid><oa>free_for_read</oa></addata></record>
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identifier ISSN: 0197-4580
ispartof Neurobiology of aging, 2017-01, Vol.49, p.217.e1-217.e4
issn 0197-4580
1558-1497
language eng
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source MEDLINE; Elsevier ScienceDirect Journals; SWEPUB Freely available online
subjects Epistasis, Genetic
Epistasis, Genetic - genetics
Genetic Association Studies
Genetic epidemiology
Genetic Loci
Genetic Loci - genetics
Genetic Predisposition to Disease
Genetic Predisposition to Disease - genetics
Genetic Variation
Genetic Variation - genetics
Human health and pathology
Humans
Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 - genetics
Life Sciences
LRRK2
Multicenter Studies as Topic
PARK16
Parkinson Disease
Parkinson Disease - genetics
Parkinson's disease
Risk
title Evaluation of the interaction between LRRK2 and PARK16 loci in determining risk of Parkinson's disease: analysis of a large multicenter study
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