In AD models, O-GlcNAcylation of NF-κB/p65 exerts anti-inflammatory effects: restoring O-GlcNAcylation at Ser384 in astrocytes suppresses p65 phosphorylation and nuclear translocation, reduces Aβ plaque deposition, and ameliorates cognitive deficits by attenuating NF-κB pathway activation (144). This evidence concerns the gene NFKB1 and Alzheimer disease.