We compared proteomic readout of three mouse models of amyloidosis at different ages, with early and late symptoms (Fig. 1a, Supplementary Table 1): (i) 5xFAD (3-, 6-, 12-month-old), overexpressing human APP and PSEN1 genes carrying a total of five human disease mutations under the Thy1 promoter, which promotes rapid onset of amyloid pathology25; (ii) NLF (3-, 12-month-old, with weak pathology) and NLGF (3-, 6-, 12-, 18-month-old, with strong pathology), both being next-generation knock-in models with humanized Aβ without gene overexpression28. The gene discussed is PSEN1; the disease is amyloidosis.