NFKB1 and Alzheimer disease: At the same time, reactive glia and activated macrophages, which operate in the “NF-kB mode”, are expected to upregulate both TGF-beta secretion and TGF-beta receptor expression (in addition to other growth factors, cytokines, and their receptors) and to move toward sources of A-beta and oxidative stress (“wounds”), thereby leading to the plaque-associated gliosis, inflammation, and the overall increased levels of TGF-beta in AD brains, which is also observed [46, 47], adding to confusion.