In addition to IL-1β induction of the precursors of the principal neuropathological changes in AD, viz., APP [23] for Aβ plaques, S100B for non-sensical growth of dystrophic neurites in plaques [41], synthesis and activation of MAPK-p38 for hyperphosphorylation of tau [42,43], favors formation of neurofibrillary tangles. Here, IL1B is linked to Alzheimer disease.