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

页码：1440 / 1442

页数：3

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