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No association between an intronic biallelic polymorphism of the FE65 gene and Alzheimer's disease

Papassotiropoulos, A. and Bagli, M. and Becker, K. and Jessen, F. and Maier, W. and Rao, M. L. and Ludwig, M. and Heun, R.. (2000) No association between an intronic biallelic polymorphism of the FE65 gene and Alzheimer's disease. International journal of molecular medicine, Vol. 6, H. 5. pp. 587-589.

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Official URL: http://edoc.unibas.ch/dok/A5257210

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Abstract

The cleavage of the amyloid precursor protein (APP) into amyloidogenic components (Abeta) is a central event in the pathogenesis of Alzheimer's disease (AD). FE65 is a protein that is involved in APP metabolism and may facilitate the production of Abeta. Recently, an intronic polymorphism of the gene encoding FE65 (FE65) was associated with altered risk for the development of sporadic AD. In our sample of 102 AD patients and 351 non-demented controls we did not replicate the association between FE65 and AD. Moreover, we observed no risk-modifying interaction and no linkage disequilibrium between FE65 and the gene encoding the acid protease cathepsin D (catD), which - like FE65 - is involved in APP metabolism and is also located on chromosome 11p15. We conclude that, whereas FE65 is implicated in AD pathology, the gene encoding FE65 does not appear to confer a substantial risk for AD.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum > Services Biozentrum > Life Sciences Training Facility (Papassotiropoulos)
07 Faculty of Psychology > Departement Psychologie > Forschungsbereich Klinische Psychologie und Neurowissenschaften > Molecular Psychology (Papassotiropoulos)
UniBasel Contributors:Papassotiropoulos, Andreas
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:04 Sep 2015 14:31
Deposited On:22 Mar 2012 13:50

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