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Cellular Prion Protein Mediates Impairment of Synaptic Plasticity by Amyloid-β Oligomers

A pathological hallmark of Alzheimer’s disease (AD) is an accumulation of insoluble plaque containing the amyloid-β peptide (Aβ) of 40–42 aa residues1. Prefibrillar, soluble oligomers of Aβ have been recognized to be early and key intermediates in AD-related synaptic dysfunction2–9. At nanomolar con...

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Detalles Bibliográficos
Autores principales:	Laurén, Juha, Gimbel, David A., Nygaard, Haakon B., Gilbert, John W., Strittmatter, Stephen M.
Formato:	Texto
Lenguaje:	English
Publicado:	2009
Materias:	Article
Acceso en línea:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748841/ https://www.ncbi.nlm.nih.gov/pubmed/19242475 http://dx.doi.org/10.1038/nature07761

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