Quick Search:

uzh logo
Browse by:

Zurich Open Repository and Archive

Maintenance: Tuesday, 5.7.2016, 07:00-08:00

Maintenance work on ZORA and JDB on Tuesday, 5th July, 07h00-08h00. During this time there will be a brief unavailability for about 1 hour. Please be patient.

Benussi, L; Ghidoni, R; Steinhoff, T; Alberici, A; Villa, A; Mazzoli, F; Nicosia, F; Barbiero, L; Broglio, L; Feudatari, E; Signorini, S; Finckh, U; Nitsch, R M; Binetti, G (2003). Alzheimer disease-associated cystatin C variant undergoes impaired secretion. Neurobiology of Disease, 13(1):15-21.

Full text not available from this repository.

View at publisher


CST3 is the coding gene for cystatin C (CysC). CST3 B/B homozygosity is associated with an increased risk of developing Alzheimer disease. We performed CysC analysis on human primary skin fibroblasts obtained from donors carrying A/A, A/B, and B/B CST3. Pulse-chase experiments demonstrated that the release of the B variant of CysC has a different temporal pattern compared to that of the A one. Fibroblasts B/B homozygous displayed a reduced secretion of CysC due to a less efficient cleavage of the signal peptide, as suggested by high-resolution Western blot analysis and by in vitro assay. In the brain, the reduced level of CysC may represent the molecular factor responsible for the increased risk of Alzheimer disease.


39 citations in Web of Science®
44 citations in Scopus®
Google Scholar™


Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Psychiatric University Hospital Zurich > Division of Psychiatric Research and Clinic for Psychogeriatric Medicine
Dewey Decimal Classification:610 Medicine & health
Deposited On:08 Sep 2011 06:45
Last Modified:05 Apr 2016 15:00
Publisher DOI:10.1016/S0969-9961(03)00012-3
PubMed ID:12758063

Users (please log in): suggest update or correction for this item

Repository Staff Only: item control page