Reference : Modulation of disease risk according to a cathepsin D / apolipoprotein E genotype in ...
Scientific journals : Article
Life sciences : Genetics & genetic processes
http://hdl.handle.net/10993/17129
Modulation of disease risk according to a cathepsin D / apolipoprotein E genotype in Parkinson's disease.
English
Schulte, T. [> >]
Bohringer, S. [> >]
Schols, L. [> >]
Muller, T. [> >]
Fischer, C. [> >]
Riess, O. [> >]
Przuntek, H. [> >]
Berger, K. [> >]
Epplen, J. T. [> >]
Krüger, Rejko mailto [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit]
2003
Journal of neural transmission (Vienna, Austria : 1996)
110
7
749-55
Yes (verified by ORBilu)
0300-9564
Austria
[en] Aged ; Apolipoproteins E/genetics ; Cathepsin D/genetics ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Male ; Middle Aged ; Parkinson Disease/genetics
[en] Aspartyl protease Cathepsin D (CTSD) has been suggested to play a role in the pathogenesis of sporadic Alzheimer's disease (AD) due to interference with protein degradation mechanisms. A C224T (A38V) polymorphism in exon 2 of the CTSD gene is reported to be associated with an increased risk for AD. The partially overlapping pathology between AD and Parkinson's disease (PD) led us to investigate the role of this polymorphism in PD. Using association studies in 457 German PD patients and 340 controls we found no evidence for direct association between the CTSD genotype and PD. However, stratification for the apolipoprotein E (APOE) epsilon4 allele suggests a protective effect of the CTSD T-allele in PD (OR = 0.24, p = 0.002). Our findings suggest interference of CTSD and APOE polymorphisms in the pathogenesis of PD, in the sense of modulating disease risk.
Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group)
http://hdl.handle.net/10993/17129
10.1007/s00702-003-0832-x

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