As mentioned earlier, the excessive activation of GSK3β not only mediates the degradation of Nrf2, but also participates in tau hyperphosphorylation, Aβ aggregation-related neuroinflammation (Hooper et al. 2008), making it a possible reason for the decreased Nrf2 activity in AD (Lane et al. 2021). This evidence concerns the gene GSK3B and Alzheimer disease.