TML-6 was found to effectively inhibit multiple pathways of AD pathogenesis, including the inhibition of the synthesis of APP and Aβ, the upregulation of levels of ApoE, the suppression of the inflammation-related phosphorylated NF-κB and the aging-related mTOR, and the increase in the expression of the anti-oxidative stress gene Nrf2. This evidence concerns the gene NFKB1 and Alzheimer disease.