Brief Communication abstract


Nature Neuroscience 12, 119 - 121 (2008)
Published online: 4 January 2009 | doi:10.1038/nn.2240

Collagen VI protects neurons against Abold beta toxicity

Jason S Cheng1,6, Dena B Dubal1,2,6, Daniel H Kim1, Justin Legleiter1,2,5, Irene H Cheng1,2,5, Gui-Qiu Yu1, Ina Tesseur3, Tony Wyss-Coray3, Paolo Bonaldo4 & Lennart Mucke1,2

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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.

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  1. Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, California 94158, USA.
  2. Department of Neurology, University of California, San Francisco, 1650 Owens Street, San Francisco, California 94158, USA.
  3. Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.
  4. University of Padova, Viale G. Colombo 3, I-35100 Padova, Italy.
  5. Present addresses: Department of Chemistry, West Virginia University, Morgantown, West Virginia 26506, USA (J.L.), and National Yang Ming University, Institute of Brain Science, 155 Li-Nong Street, Section 2 Shi-Pai, Taipei, R.O.C. (I.H.C.).
  6. These authors contributed equally to this work.

Correspondence to: Lennart Mucke1,2 e-mail: lmucke@gladstone.ucsf.edu




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