An N-terminal Fragment of the Prion Protein Binds to Amyloid-β Oligomers and Inhibits Their Neurotoxicity in Vivo

A hallmark of Alzheimer disease (AD) is the accumulation of the amyloid-β (Aβ) peptide in the brain. Considerable evidence suggests that soluble Aβ oligomers are responsible for the synaptic dysfunction and cognitive deficit observed in AD. However, the mechanism by which these oligomers exert their...

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Bibliografiske detaljer
Main Authors: Fluharty, Brian R., Biasini, Emiliano, Stravalaci, Matteo, Sclip, Alessandra, Diomede, Luisa, Balducci, Claudia, La Vitola, Pietro, Messa, Massimo, Colombo, Laura, Forloni, Gianluigi, Borsello, Tiziana, Gobbi, Marco, Harris, David A.
Format: Artigo
Sprog:Inglês
Udgivet: American Society for Biochemistry and Molecular Biology 2013
Fag:
Molecular Bases of Disease
Online adgang:https://ncbi.nlm.nih.gov/pmc/articles/PMC3597823/
https://ncbi.nlm.nih.gov/pubmed/23362282
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1074/jbc.M112.423954
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