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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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| Main Authors: | , , , , |
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| Format: | Artigo |
| Sprog: | Inglês |
| Udgivet: |
2009
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| Fag: | |
| Online adgang: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2748841/ https://ncbi.nlm.nih.gov/pubmed/19242475 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/nature07761 |
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