Brief Communication abstract
Nature Genetics 39, 1440 - 1442 (2007)
Published online: 18 November 2007 | doi:10.1038/ng.2007.29
Cystatin C inhibits amyloid-
deposition in Alzheimer's disease mouse models
Weiqian Mi1, Monika Pawlik1,2, Magdalena Sastre2,5, Sonia S Jung1,5, David S Radvinsky1, Andrew M Klein1, John Sommer1, Stephen D Schmidt1, Ralph A Nixon1,3,4, Paul M Mathews1,3 & Efrat Levy1,2,3
Using transgenic mice expressing human cystatin C (encoded by CST3), we show that cystatin C binds soluble amyloid-
peptide and inhibits cerebral amyloid deposition in amyloid- precursor protein (APP) transgenic mice. Cystatin C expression twice that of the endogenous mouse cystatin C was sufficient to substantially diminish amyloid- deposition. Thus, cystatin C has a protective role in Alzheimer's disease pathogenesis, and modulation of cystatin C concentrations may have therapeutic implications for the disease.
- Nathan S. Kline Institute, Orangeburg, New York 10962, USA.
- Department of Pharmacology, New York University School of Medicine, New York, New York 10016, USA.
- Department of Psychiatry, New York University School of Medicine, New York, New York 10016, USA.
- Department of Cell Biology, New York University School of Medicine, New York, New York 10016, USA.
- Present addresses: Department of Cellular and Molecular Neuroscience, Imperial College London, London W12 0NN, UK (M.S.) and Centocor Research and Development Inc., Radnor, Pennsylvania 19087, USA (S.S.J.).
Correspondence to: Efrat Levy1,2,3 e-mail: elevy@nki.rfmh.org
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RESEARCH
Cystatin C modulates cerebral β-amyloidosisNature Genetics Brief Communication (01 Dec 2007)
