Cystatin C inhibits amyloid-β deposition in Alzheimer's disease mouse models

被引：161
|
作者：
Mi, Weiqian
Pawlik, Monika
Sastre, Magdalena
Jung, Sonia S.
Radvinsky, David S.
Klein, Andrew M.
Sommer, John
Schmidt, Stephen D.
Nixon, Ralph A.
Mathews, Paul M.
Levy, Efrat [1 ]
机构：
[1] Nathan S Kline Inst, Orangeburg, NY 10962 USA
[2] NYU, Sch Med, New York, NY 10016 USA
[3] Centocor Res & Dev Inc, Radnor, PA 19087 USA
来源：
NATURE GENETICS | 2007年 / 39卷 / 12期
关键词：
D O I：
10.1038/ng.2007.29
中图分类号：
Q3 [遗传学];
学科分类号：
071007 ; 090102 ;
摘要：
Using transgenic mice expressing human cystatin C ( encoded by CST3), we show that cystatin C binds soluble amyloid-beta peptide and inhibits cerebral amyloid deposition in amyloid-beta precursor protein ( APP) transgenic mice. Cystatin C expression twice that of the endogenous mouse cystatin C was sufficient to substantially diminish amyloid-beta 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.
引用
收藏
页码：1440 / 1442
页数：3
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