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The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Genetic polymorphism of cathepsin D is strongly associated with the risk for developing sporadic Alzheimer's disease

Papassotiropoulos, Andreas, Bagli, Metin, Feder, Oliver, Jessen, Frank, Maier, Wolfgang, Rao, Marie Luise, Ludwig, Michael, Schwab, Sibylle G, Heun, Reinhard·1999·Neuroscience Letters
DOI 10.1016/s0304-3940(99)00071-3
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Abstract

The beta amyloid peptide derives from its precursor protein via proteolytic cleavage of yet unidentified proteases (beta- and gamma-secretases). Cathepsin D is an intracellular protease with in-vitro beta-secretase-like features. An exonic polymorphism of the cathepsin D gene (alanine to valine transition at position 224, exon 2) has been associated with altered enzyme function. We tested the hypothesis that this polymorphism is associated with an increased risk for Alzheimer's disease in 102 demented patients, 191 healthy subjects, and 160 depressed patients. There was a highly significant overrepresentation of the cathepsin D*T allele in demented patients (14.2%) compared to non-demented controls (6.7%, P = 0.0012). Carriers of the cathepsin D*T allele had a 2.4-fold increased risk for developing AD than non-carriers. Carriers of the apolipoprotein E epsilon 4 allele had a 4.1 -fold increased risk than non-carriers. The odds ratio for subjects with the apolipoprotein E epsilon 4 and the cathepsin D*T allele was 5.9. Our data suggest that the cathepsin D genotype is strongly associated with the risk for Alzheimer's disease.

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Crossref · 10.1016/s0304-3940(99)00071-3

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  • Polymorphisms in several lysosomal cathepsin genes are associated with increased AD susceptibility.

    “Genetic studies further support lysosomal involvement, as polymorphisms in several lysosomal cathepsin genes are associated with increased AD susceptibility (Bhojak et al. 2001), (Papassotiropoulos et al. 1999).”

    From TMEM55B downregulation promotes neurodegeneration in Alzheimer’s disease models (2026) · cites this paper as Papassotiropoulos et al. 1999

  • Cathepsin polymorphisms increase AD risk, whereas cystatin B/C deletion improves phenotypes.

    “Cathepsin polymorphisms increase AD risk (Bhojak et al. 2001), (Papassotiropoulos et al. 1999), whereas cystatin B/C deletion improves phenotypes (Mi et al. 2007), (Yang et al. 2011), (Yang et al. 2014).”

    From TMEM55B downregulation promotes neurodegeneration in Alzheimer’s disease models (2026) · cites this paper as Papassotiropoulos et al. 1999

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Research works printed but not linked: 18

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Metadata

Authors
Papassotiropoulos, A., Bagli, M., Feder, O., Jessen, F., Maier, W., Rao, M. L., Ludwig, M., Schwab, S. G., & Heun, R.
Venue
Neuroscience Letters
Publisher
Elsevier BV
Published
1999-03
Volume
262
Issue
3
Pages
171-174
ISSN
0304-3940
DOI
10.1016/s0304-3940(99)00071-3
Cited by
53
References
2
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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