期刊
NATURE NEUROSCIENCE
卷 12, 期 2, 页码 119-121出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.2240
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资金
- US National Institutes of Health
- Howard Hughes Medical Institute
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.
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