@article{0e4476cc368f4d2dbfeaceed7c7a3372,
title = "Collagen VI protects neurons against Aβ toxicity",
abstract = "Amyloid-β (Aβ) 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 Aβ neurotoxicity, whereas treatment of neurons with soluble collagen VI blocked the association of Aβ oligomers with neurons, enhanced Aβ aggregation and prevented neurotoxicity. These results identify collagen VI as an important component of the neuronal injury response and demonstrate its neuroprotective potential.",
author = "Cheng, {Jason S.} and Dubal, {Dena B.} and Kim, {Daniel H.} and Justin Legleiter and Cheng, {Irene H.} and Yu, {Gui Qiu} and Ina Tesseur and Tony Wyss-Coray and Paolo Bonaldo and Lennart Mucke",
note = "Funding Information: We thank H. Solanoy, X. Wang, G.-Q. Yu and Y. Zhou for excellent technical support, S. Maeda for helpful discussions on AFM, P. Scherer for a1(VI)-deficient mice, R. Jaenisch for CamK-Cre93 transgenic mice, H. Moses for TbRIIfl/fl knockin mice, C. Weissmann for APP-deficient mice, M.-L. Chu for the Col6a1 cDNA, the New York Brain Bank at Columbia University Medical Center for human tissues, G. Howard and S. Ordway for editorial review, J. Carroll, T. Roberts and C. Goodfellow for preparation of graphics, and D. McPherson for administrative assistance. Confocal images were acquired at the Nikon Imaging Center at University of California, San Francisco. This work was supported by grants from the US National Institutes of Health, a medical student fellowship from the Howard Hughes Medical Institute, a Larry L. Hillblom Fellowship and a facilities grant from the National Center for Research Resources.",
year = "2009",
month = feb,
doi = "10.1038/nn.2240",
language = "English",
volume = "12",
pages = "119--121",
journal = "Nature Neuroscience",
issn = "1097-6256",
publisher = "Nature Publishing Group",
number = "2",
}