The key element in this hypothesis is an endocytosis-associated mechanism that depends on tau-fyn interaction, induces tau oligomerization and is potentiated by both the activity of excitotoxicity-prone synapses and the progressive failure of tau to segregate normally to the axon in tauopathy pathogenesis, which increases the exposure of dendritic elements to tau, thereby amplifying perisynaptic tau toxicity [Ref. Here, FYN is linked to tauopathy.