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...

Πλήρης περιγραφή

Αποθηκεύτηκε σε:
Λεπτομέρειες βιβλιογραφικής εγγραφής
Κύριοι συγγραφείς: 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.
Μορφή: Artigo
Γλώσσα:Inglês
Έκδοση: American Society for Biochemistry and Molecular Biology 2013
Θέματα:
Molecular Bases of Disease
Διαθέσιμο Online: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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