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Human Molecular Genetics Advance Access published online on October 15, 2008
Human Molecular Genetics, 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,§, Javier Simón-Sánchez1,3,§, 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 Department of Public Health Sciences, Center for Public Health Genomics, University of Virginia, Charlottesville, VA 22908, USA

* To whom correspondence should be addressed. Tel: +1 301 451 6079; Fax: +1 301 451 5466; E-Mail: singleta{at}mail.nih.gov . Laboratory of Neurogenetics, NIA IRP NIH, Room 1A1014 Building 35, 35 Lincoln drive, Bethesda, MD 20892, USA

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 independents populations, we sequenced the entire coding region of GIGYF2 in a large series of Portuguese and a 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.

§ These authors contributed equally to this work.


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