Many of these pro-resilience proteins that were decreased in 5xFAD PV-INs (e.g. Cplx1, Cplx2, Elfn1, Rab3c, Rtn4, Dlgap4, Sorbs1, Magi1) were also highly-enriched in PV-INs as compared to Camk2a neurons (Fig. 5P, Supplementary Fig. 10E, F), indicating that the changes in early AD pathology may indeed be related to PV-IN dysfunction. This evidence concerns the gene RAB3C and Alzheimer disease.