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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Detalhes bibliográficos
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.
Formato: Artigo
Idioma:Inglês
Publicado em: American Society for Biochemistry and Molecular Biology 2013
Assuntos:
Molecular Bases of Disease
Acesso em linha: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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