FYN and Alzheimer disease: Scheme 6 illustrates the early, synaptic toxic effects of Aβ oligomers. On the other hand, higher concentrations of oligomers lead to increased binding to PrPC, increased NMDAR phosphorylation, the greater opening of the ion channel of this receptor, and increased excitotoxicity due to increased excitotoxicity to a significant influx of Ca2+ to neurons. Aβ–pTau–Fyn interactions are viewed as a toxic synaptic triad in the pathomechanism of AD [67]. Synaptic dysfunction can be induced by Aβ binding to receptors located in synapses, such as NMDAR, AChR and mGluR5 [47,67].