摘要

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

  • 出版日期2013-2