Collagen VI protects neurons against Aβ toxicity

被引：107

作者：

Cheng, Jason S. ^{[1
]}

Dubal, Dena B. ^{[1
,2
]}

Kim, Daniel H. ^{[1
]}

Legleiter, Justin ^{[1
,2
]}

Cheng, Irene H. ^{[1
,2
]}

Yu, Gui-Qiu ^{[1
]}

Tesseur, Ina ^{[3
]}

Wyss-Coray, Tony ^{[3
]}

Bonaldo, Paolo ^{[4
]}

Mucke, Lennart ^{[1
,2
]}

机构：

[1] Gladstone Inst Neurol Dis, San Francisco, CA 94158 USA

[2] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94158 USA

[3] Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA

[4] Univ Padua, I-35100 Padua, Italy

来源：

NATURE NEUROSCIENCE | 2009年 / 12卷 / 02期

基金：

美国国家卫生研究院;

关键词：

AMYLOID PRECURSOR PROTEIN; MOUSE; DEFICIENCY; EXPRESSION; MICE;

D O I：

10.1038/nn.2240

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Amyloid-beta (A beta) peptides, widely presumed to cause Alzheimer's disease, increased mouse neuronal expression of collagen VI through a mechanism involving transforming growth factor signaling. Reduction of collagen VI augmented A beta neurotoxicity, whereas treatment of neurons with soluble collagen VI blocked the association of A beta oligomers with neurons, enhanced A beta aggregation and prevented neurotoxicity. These results identify collagen VI as an important component of the neuronal injury response and demonstrate its neuroprotective potential.

引用

页码：119 / 121

页数：3

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