TML-6 exhibited multiple biological effects on combining aging biology and AD pathogenesis, including the inhibition of APP and Aβ synthesis, the upregulation of ApoE, the transcriptional activation of the anti-oxidative Nrf2 gene, the suppression of phospho-mTOR, and the inhibition of proinflammatory phospho-NF-κB. Here, NFE2L2 is linked to Alzheimer disease.