NFKB1 and Alzheimer disease: Key findings demonstrate HSN-S1’s ability to (1) suppress pro-inflammatory cytokines, (2) modulate critical signaling pathways (ERK, p38 MAPK, NF-κB), (3) act on various AD-relevant cell types (keratinocytes, macrophages, CD4+ T cells), (4) inhibit S. aureus growth, a pivotal aspect of AD pathology, and (5) modulate cytokines through NFAT and NF-κB pathways.