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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محفوظ في:
التفاصيل البيبلوغرافية
المؤلفون الرئيسيون: 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.
التنسيق: Artigo
اللغة:Inglês
منشور في: American Society for Biochemistry and Molecular Biology 2013
الموضوعات:
Molecular Bases of Disease
الوصول للمادة أونلاين: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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