Brief Communication abstract
Nature Genetics 39, 1437 - 1439 (2007)
Published online: 18 November 2007 | doi:10.1038/ng.2007.23
Cystatin C modulates cerebral 
-amyloidosis
Stephan A Kaeser1, Martin C Herzig1, Janaky Coomaraswamy1, Ellen Kilger1, Maj-Linda Selenica2, David T Winkler3, Matthias Staufenbiel4, Efrat Levy5, Anders Grubb2 & Mathias Jucker1
The CST3 Thr25 allele of CST3, which encodes cystatin C, leads to reduced cystatin C secretion and conveys susceptibility to Alzheimer's disease. Here we show that overexpression of human cystatin C in brains of APP-transgenic mice reduces cerebral amyloid-
deposition and that cystatin C binds amyloid- and inhibits its fibril formation. Our results suggest that cystatin C concentrations modulate cerebral amyloidosis risk and provide an opportunity for genetic risk assessment and therapeutic interventions.
- Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tübingen, Otfried-Müller Strasse 27, D-72076 Tübingen, Germany.
- Department of Clinical Chemistry, Lund University Hospital, 22185 Lund, Sweden.
- Department of Neuropathology, Institute of Pathology, University of Basel, CH-4003 Basel, Switzerland.
- Novartis Institutes for Biomedical Research Basel, Nervous System, CH-4002 Basel, Switzerland.
- Departments of Psychiatry and Pharmacology, New York University School of Medicine, New York, New York 10016, USA and Nathan Kline Institute, Orangeburg, New York 10962, USA.
Correspondence to: Mathias Jucker1 e-mail: mathias.jucker@uni-tuebingen.de
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