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Human Molecular Genetics Advance Access originally published online on October 15, 2008
Human Molecular Genetics 2009 18(2):341-346; doi:10.1093/hmg/ddn340
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Published by Oxford University Press 2008

Lack of replication of association between GIGYF2 variants and Parkinson disease

Jose Bras1,2,{dagger}, Javier Simón-Sánchez1,3,{dagger}, Monica Federoff1, Ana Morgadinho4, Cristina Januario4, Maria Ribeiro4, Luis Cunha4, Catarina Oliveira2,4 and Andrew B. Singleton1,5,*

1 Laboratory of Neurogenetics, Intramural Research Program, National Institute on Aging, Bethesda, MD 20892, USA 2 Center for Neurosciences and Cell Biology, University of Coimbra, 3000 Coimbra, Portugal 3 Unidad de Genética Molecular, Departamento de Genómica y Proteómica, Instituto de Biomedicina de Valencia-CSIC, 46010 Valencia, Spain 4 Neurology Service, Coimbra University Hospital, 3000 Coimbra, Portugal 5 Center for Public Health Genomics, Department of Public Health Sciences, University of Virginia, Charlottesville, VA 22908, USA

* To whom correspondence should be addressed at: Laboratory of Neurogenetics, NIA IRP NIH, Room 1A1014, Building 35, 35 Lincoln Drive, Bethesda, MD 20892, USA. Tel: +1 3014516079; Fax: +1 3014515466; Email: singleta{at}mail.nih.gov

Received September 1, 2008; Revised October 6, 2008; Accepted October 13, 2008

Mutations in GIGYF2 have recently been described as causative of Parkinson's disease in Europeans. In an attempt to replicate these results in independent populations, we sequenced the entire coding region of GIGYF2 in a large series of Portuguese and North American samples. We report the finding of two of the previously published mutations in neurologically normal Control individuals. This suggests that mutations in GIGYF2 are not strongly related to the development of the disease in either of these populations.


{dagger} The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.


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