Skip Navigation


Human Molecular Genetics Advance Access originally published online on June 25, 2008
Human Molecular Genetics 2008 17(18):2863-2867; doi:10.1093/hmg/ddn183
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Data
Right arrow All Versions of this Article:
17/18/2863    most recent
ddn183v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Chapuis, J.
Right arrow Articles by Lambert, J.-C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chapuis, J.
Right arrow Articles by Lambert, J.-C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Association study of the NEDD9 gene with the risk of developing Alzheimer's and Parkinson's disease

Julien Chapuis1, Frédéric Moisan2,3, Georges Mellick4, Alexis Elbaz2,3, Peter Silburn4, Florence Pasquier5, Didier Hannequin6, Corinne Lendon7, Dominique Campion6, Philippe Amouyel1 and Jean-Charles Lambert1,*

1 Inserm, U744, Institut Pasteur de Lille, Université de Lille 2, Lille, France 2 Inserm, U708, Hôpital de la Salpêtrière, Paris, France 3 Université Pierre et Marie Curie-Paris6, Paris, France 4 Eskitis Institue for Cell and Molecular Therapies, Griffith University, Queensland, Australia 5 EA2391, Department of Neurology, Memory Clinic, University Hospital of Lille, Lille, France 6 Inserm, U614, Faculty of Medicine, IFRMP, Rouen, France 7 Molecular Psychiatry Group, Queensland Institute of Medical Research, Brisbane, Australia

* To whom correspondence should be addressed at: unité INSERM 744, Institut Pasteur de Lille, BP 245, 1, rue du professeur Calmette, 59019 Lille cédex, France. Tel: +33 320 877391; Fax: +33 320 877894; Email: jean-charles.lambert{at}pasteur-lille.fr

Received May 26, 2008; Accepted June 22, 2008

Alzheimer's disease (AD) and Parkinson's disease (PD), the two most common neurodegenerative disorders in the elderly, have been hypothesized to share genetic determinants. Recently, Li et al. proposed that a variant in the NEDD9 gene may be one of these common genetic factors. We attempted to confirm this initial observation by conducting an equivalent analysis in terms of pathologies and sample size. We genotyped the NEDD9 rs760678 SNP in three independent AD case–control studies (n = 3176) and two independent PD case–control studies (n = 1855). However, we failed to detect an association of this SNP with the risk of developing AD or PD, in any of these populations. In conclusion, these data indicate that the rs760678 SNP of the NEDD9 gene is at best a weak genetic determinant of AD or PD.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cereb CortexHome page
T. Vogel, S. Ahrens, N. Buttner, and K. Krieglstein
Transforming Growth Factor {beta} Promotes Neuronal Cell Fate of Mouse Cortical and Hippocampal Progenitors In Vitro and In Vivo: Identification of Nedd9 as an Essential Signaling Component
Cereb Cortex, July 8, 2009; (2009) bhp134v1.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.