Secondly, as long-term administration of indomethacin, a key inhibitor of the inflammatory mediator NF-κB, significantly reduces cerebral amyloidosis in Tg2576 mice [139], and NF-κB is downstream of S100B [58], it is possible that arundic acid-induced inhibition of NF-κB activity may mitigate amyloidosis in Tg2576 mice. This evidence concerns the gene NFKB1 and amyloidosis.