In turn, the elevated Nrf2 affected SOD, CAT, MDA and GSH-PX, reversing the decrease in SOD, CAT and GSH-PX activity and increase in MDA, thereby counteracting DM-induced ERS and OS and reducing PDI as well as misfolded protein production, the degree of neuronal apoptosis and degeneration and the production of Aβ plaques, indicating that Trx-1 has antidiabetic effects and opposes AD-like changes (see Figures 4, 6). This evidence concerns the gene NFE2L2 and diabetes mellitus.