Skip Navigation



Human Molecular Genetics Advance Access published online on October 28, 2003
Human Molecular Genetics, doi:10.1093/hmg/ddg361
© 2003 by Oxford University Press
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
13/1/47    most recent
ddg361v1
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 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 arrowRequest Permissions
Google Scholar
Right arrow Articles by de Quervain, D. J.-F.
Right arrow Articles by Papassotiropoulos, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by de Quervain, D. J.-F.
Right arrow Articles by Papassotiropoulos, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

©2003 Oxford University Press

Article

Glucocorticoid-related genetic susceptibility for Alzheimer's disease

Dominique J.-F. de Quervain 1*, Raphael Poirier 1, M. Axel Wollmer 1, Luigi M.E. Grimaldi 2, Magdalini Tsolaki 3, Johannes R. Streffer 1, Christoph Hock 1, Roger M. Nitsch 1, M. Hasan Mohajeri 1, and Andreas Papassotiropoulos 1*

1 Division of Psychiatry Research, University of Zürich, Lenggstr. 31, 8029 Zürich, Switzerland
2 Department of Neuroscience, AUSL n.2, Caltanissetta, Italy; Neuroimmunology Unit, Department of Neuroscience, IRCCS H. San Raffaele, Milan, Italy
3 Third Department of Neurology, Aristotle University of Thessaloniki, Greece

* To whom correspondence should be addressed. E-mail: papas{at}bli.unizh.ch.


  Abstract

Because glucocorticoid excess increases neuronal vulnerability, genetic variations in the glucocorticoid system may be related to the risk for Alzheimer's disease (AD). We analyzed single nucleotide polymorphisms (SNPs) in ten glucocorticoid-related genes in a population of 814 AD patients and unrelated control subjects. Set-association analysis revealed that a rare haplotype in the 5' regulatory region of the gene encoding 11{beta}-hydroxysteroid dehydrogenase type 1 (HSD11B1) was associated with a six-fold increased risk for sporadic AD. Results of a reporter-gene assay indicated that the rare risk-associated haplotype altered HSD11B1 transcription. HSD11B1 controls tissue levels of biologically active glucocorticoids and thereby influences neuronal vulnerability. Our results indicate that a functional variation in the glucocorticoid system increases the risk for AD which may have important implications for the diagnosis and treatment of this disease.


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
 J. Neurosci.Home page
K. N. Green, L. M. Billings, B. Roozendaal, J. L. McGaugh, and F. M. LaFerla
Glucocorticoids Increase Amyloid-beta and Tau Pathology in a Mouse Model of Alzheimer's Disease.
J. Neurosci., August 30, 2006; 26(35): 9047 - 9056.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
R. M. de Pablos, R. F. Villaran, S. Arguelles, A. J. Herrera, J. L. Venero, A. Ayala, J. Cano, and A. Machado
Stress Increases Vulnerability to Inflammation in the Rat Prefrontal Cortex
J. Neurosci., May 24, 2006; 26(21): 5709 - 5719.
[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.