JUN and Alzheimer disease: Previously, it has been shown that ChLNs bearing the mutation I416T in PSEN1 reproduce the typical neuropathology of AD, characterized by the accumulation of iAβ and the phosphorylation of TAU at Ser202/Thr205 conjointly with the generation of H2O2, oxidation of DJ-1, phosphorylation of c-JUN at Ser63/Ser73, loss of ΔΨm, overexpression of TP53 and cleaved caspase 3 (CC3), and failure to respond to ACh-induced Ca2+ influx (Figure 13, [33]).