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Prion. 2013 Jan-Feb;7(1):37-41. doi: 10.4161/pri.22212. Epub 2012 Sep 17.

Amyloid-β induced signaling by cellular prion protein and Fyn kinase in Alzheimer disease.

Author information

1
Cellular Neuroscience, Neurodegeneration and Repair Program, Department of Neurology, Yale University School of Medicine, New Haven, CT, USA.

Abstract

Alzheimer disease (AD) is the most prevalent cause of dementia. Amyloid-β (Aβ) oligomers are potent synaptotoxins thought to mediate AD-related phenotypes. Cellular prion protein (PrP(C)) has been identified as a high-affinity receptor for Aβ oligomers. Herein, we review the functional consequences of Aβ oligomer binding to PrP(C) on the neuronal surface. We highlight recent evidence that Fyn kinase mediates signal transduction downstream of the PrP(C)-Aβ oligomer complex. These studies suggest that PrP(C) has a central role in AD pathogenesis and may provide a target for therapeutic intervention in AD.

KEYWORDS:

Alzheimer disease; Fyn kinase; PrpC; cellular prion protein; prion

PMID:
22987042
PMCID:
PMC3609048
DOI:
10.4161/pri.22212
[Indexed for MEDLINE]
Free PMC Article
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