Cystatin C modulates cerebral β-amyloidosis
Cystatin C modulates cerebral β-amyloidosis
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DOI：
10.1038/ng.2007.23
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发表时间：
2007-12-01
期刊：
影响因子：
30.8
通讯作者：
Jucker, Mathias
中科院分区：
文献类型：
--
作者：
Kaeser, Stephan A.;Herzig, Martin C.;Jucker, Mathias
CST3的CST3 Thr25等位基因编码胱抑素C，导致胱抑素C分泌减少，并传递对阿尔茨海默病的易感性。本研究表明，在app转基因小鼠的大脑中，人胱抑素C的过表达减少了大脑淀粉样蛋白- β的沉积，并且胱抑素C与淀粉样蛋白- β结合并抑制其纤维的形成。我们的研究结果表明，胱抑素C浓度可调节脑淀粉样变性的风险，并为遗传风险评估和治疗干预提供了机会。
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.