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
收藏
页码：119 / 121
页数：3
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