Summary.
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) ε4 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.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
Author information
Authors and Affiliations
Additional information
Received December 12, 2002; accepted March 6, 2003 Published online May 5, 2003
Acknowledgements This study has been supported in part by the German Research Society (Deutsche Forschungs Gemeinschaft, grant: Scho754/2-1 to L.S. and R.K.). The MEMO-Study is supported by the German Research Society (Deutsche Forschungs Gemeinschaft, grant: BE1996/1-1).
Authors' address: Dr. R. Krüger, Department of Neurology, Neurodegeneration Laboratory, University of Tübingen, Hoppe-Seyler-Strasse 3, D-72076 Tübingen, Germany, e-mail: rejko.krueger@uni-tuebingen.de
Rights and permissions
About this article
Cite this article
Schulte, T., Böhringer, S., Schöls, L. et al. Modulation of disease risk according to a cathepsin D / apolipoprotein E genotype in Parkinson's disease. J Neural Transm 110, 749–755 (2003). https://doi.org/10.1007/s00702-003-0832-x
Issue Date:
DOI: https://doi.org/10.1007/s00702-003-0832-x