Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons.

Here the authors show that the binding of amyloid-β (Aβ) oligomers to cellular prion protein (PrPc) activates Fyn kinase. Aβ stimulation of PrPc/Fyn signaling drives phosphorylation of the NR2B subunit of NMDA receptors, with a subsequent loss of receptor surface expression and dendritic spines.