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

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 (PrPc) has been identified as a high-affinity receptor for Aβ oligomers. Herein, we review the functional consequences of Aβ oligomer binding to PrPc on the neuronal surface. We highlight recent evidence that Fyn kinase mediates signal transduction downstream of the PrPc-Aβ oligomer complex. These studies suggest that PrPC has a central role in AD pathogenesis and may provide a target for therapeutic intervention in AD.© 2012 Landes Bioscience. Do not distribute.