Collagen VI protects neurons against Aβ toxicity

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Abstract
Cheng and colleagues propose a mechanism for amyloid-β toxicity that may have relevance for Alzheimer's disease. They show that Aβ1–42 induces expression of collagen VI and that collagen VI protects against Aβ toxicity in cultured neurons. 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.