Cystatin C modulates cerebral β-amyloidosis

被引:158
作者
Kaeser, Stephan A.
Herzig, Martin C.
Coomaraswamy, Janaky
Kilger, Ellen
Selenica, Maj-Linda
Winkler, David T.
Staufenbiel, Matthias
Levy, Efrat
Grubb, Anders
Jucker, Mathias
机构
[1] Univ Tubingen, Hertie Inst Clin Brain Res, Dept Cellular Neurol, D-72076 Tubingen, Germany
[2] Univ Lund Hosp, Dept Clin Chem, S-22185 Lund, Sweden
[3] Univ Basel, Inst Pathol, Dept Neuropathol, CH-4003 Basel, Switzerland
[4] Novartis Inst Biomed Res Basel, CH-4002 Basel, Switzerland
[5] NYU, Sch Med, Dept Pharmacol & Psychiat, New York, NY 10016 USA
[6] Nathan S Kline Inst, New York, NY 10962 USA
关键词
D O I
10.1038/ng.2007.23
中图分类号
Q3 [遗传学];
学科分类号
071007 [遗传学]; 090102 [作物遗传育种];
摘要
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-beta deposition and that cystatin C binds amyloid-beta 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.
引用
收藏
页码:1437 / 1439
页数:3
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