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Human Molecular Genetics Advance Access originally published online on October 28, 2003
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Human Molecular Genetics, 2004, Vol. 13, No. 1 47-52
DOI: 10.1093/hmg/ddg361
© 2004 Oxford University Press

Glucocorticoid-related genetic susceptibility for Alzheimer's disease

Dominique J.-F. de Quervain1,*, Raphael Poirier1,{dagger}, M. Axel Wollmer1,{dagger}, Luigi M.E. Grimaldi2,3, Magdalini Tsolaki4, Johannes R. Streffer1, Christoph Hock1, Roger M. Nitsch1, M. Hasan Mohajeri1 and Andreas Papassotiropoulos1

1Division of Psychiatry Research, University of Zürich, Lenggstr. 31, 8029 Zürich, Switzerland, 2Department of Neuroscience, AUSL n. 2, Caltanissetta, Italy, 3Neuroimmunology Unit, Department of Neuroscience, IRCCS H. San Raffaele, Milan, Italy and 4Third Department of Neurology, Aristotle University of Thessaloniki, Greece

Received July 30, 2003; Accepted October 17, 2003

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 in 10 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 11ß-hydroxysteroid dehydrogenase type 1 (HSD11B1) was associated with a 6-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.

* To whom correspondence should be addressed. Tel: +41 13842601; Fax: +41 13842686; Email: quervain{at}bli.unizh.ch

{dagger} These authors contributed equally to this work.


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