Collectively, these findings showed a novel molecular mechanism in which H3K18la/NFκB axis modulates inflammation associated with aging (infammageing) by regulating SASP components IL-6 and IL-8, promoting brain aging and AD pathological phenotypes (Fig. 8).These results present potential targets for the development of drug interventions for brain aging and AD pathology. This evidence concerns the gene NFKB1 and Alzheimer disease.