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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Detalles Bibliográficos
Autores principales: 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: Online Artículo Texto
Lenguaje:English
Publicado: American Society for Biochemistry and Molecular Biology 2013
Materias:
Molecular Bases of Disease
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597823/
https://www.ncbi.nlm.nih.gov/pubmed/23362282
http://dx.doi.org/10.1074/jbc.M112.423954

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