Interestingly, in the hAPP-J20 model of AD, which, like TgA53T model of α-synucleinopathy, requires tau as a mediator of synaptic dysfunction and memory loss [94], PrPC, and Fyn activation appears to be mechanistically disconnected as tau-dependent cognitive decline in hAPP-J20 mice is unaffected by PrPC ablation [21]. The gene discussed is FYN; the disease is Alzheimer disease.