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β-amyloid oligomers and cellular prion protein in Alzheimer’s disease

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Abstract

Prefibrillar oligomers of the β-amyloid peptide (Aβ) are recognized as potential mediators of Alzheimer’s disease (AD) pathophysiology. Deficits in synaptic function, neurotoxicity, and the progression of AD have all been linked to the oligomeric Aβ assemblies rather than to Aβ monomers or to amyloid plaques. However, the molecular sites of Aβ oligomer action have remained largely unknown. Recently, the cellular prion protein (PrPC) has been shown to act as a functional receptor for Aβ oligomers in brain slices. Because PrPC serves as the substrate for Creutzfeldt–Jakob Disease (CJD), these data suggest mechanistic similarities between the two neurodegenerative diseases. Here, we review the importance of Aβ oligomers in AD, commonalities between AD and CJD, and the newly emergent role of PrPC as a receptor for Aβ oligomers.

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Acknowledgments

We thank Haakon B. Nygaard, M.D. for providing Fig. 1. S.M.S. is a member of the Kavli Institute for Neuroscience at Yale University. We acknowledge support from the National Institutes of Health, the Falk Medical Research Trust, an anonymous donor, and the Cure Alzheimer’s Fund to S.M.S.

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The authors declare that they have no conflict of interests.

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Correspondence to Stephen M. Strittmatter.

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Gunther, E.C., Strittmatter, S.M. β-amyloid oligomers and cellular prion protein in Alzheimer’s disease. J Mol Med 88, 331–338 (2010). https://doi.org/10.1007/s00109-009-0568-7

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  • DOI: https://doi.org/10.1007/s00109-009-0568-7

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