Modulation of disease risk according to a cathepsin D / apolipoprotein E genotype in Parkinson's disease

T. Schulte, S. Böhringer, L. Schöls, T. Müller, C. Fischer, O. Riess, H. Przuntek, K. Berger, J. T. Epplen, R. Krüger*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

16 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)749-755
Number of pages7
JournalJournal of Neural Transmission
Volume110
Issue number7
DOIs
Publication statusPublished - 1 Jul 2003
Externally publishedYes

Keywords

  • Apolipoprotein E
  • Cathepsin D
  • Genetics
  • Parkinson's disease

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