HDAC3 and Alzheimer disease: Previous studies have reported abnormal upregulation of HDAC3 in DNCB-induced lesional skin in AD mice, and selective inhibition of HDAC3 has been shown to relieve symptoms, suggesting its involvement in AD pathogenesis (Zhou et al., 2024), NF-κB is a central transcription factor that controls the expression of numerous inflammatory cytokines (Hayden et al., 2006).