| Literature DB >> 19122666 |
Jason S Cheng1, Dena B Dubal, Daniel H Kim, Justin Legleiter, Irene H Cheng, Gui-Qiu Yu, Ina Tesseur, Tony Wyss-Coray, Paolo Bonaldo, Lennart Mucke.
Abstract
Amyloid-beta (Abeta) 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 Abeta neurotoxicity, whereas treatment of neurons with soluble collagen VI blocked the association of Abeta oligomers with neurons, enhanced Abeta aggregation and prevented neurotoxicity. These results identify collagen VI as an important component of the neuronal injury response and demonstrate its neuroprotective potential.Entities:
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Year: 2009 PMID: 19122666 PMCID: PMC2812922 DOI: 10.1038/nn.2240
Source DB: PubMed Journal: Nat Neurosci ISSN: 1097-6256 Impact factor: 24.884