Cellular prion protein as a receptor for amyloid-β oligomers in Alzheimer's disease.

ABSTRACT: Soluble oligomers of amyloid-beta (Aβo) are implicated by biochemical and genetic evidence as a trigger for Alzheimer's disease (AD) pathophysiology. A key step is Aβo interaction with the neuronal surface to initiate a cascade of altered signal transduction leading to synaptic dysfunction and damage. This review discusses neuronal cell surface molecules with high affinity selectively for oligomeric disease-associated states of Aβ, with a particular focus on the role of cellular prion protein (PrP^C) in this process. Additional receptors may contribute to mediation of Aβo action, but PrP^C appears to play a primary role in a number of systems. The specificity of binding, the genetic necessity in mouse models of disease and downstream signaling pathways are considered. S

SUBMITTER: Salazar SV 

PROVIDER: S-EPMC5303667 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature