Notably, the absence of fractalkine signaling ameliorates Aβ plaque burden in APPPS1 transgenic mice [30], but exacerbates intraneuronal tau pathology in hTau mouse model of pure tauopathy [17], even though both events likely occur via dysregulation of IL-1β-p38 MAPK signaling pathway [19]. The gene discussed is IL1B; the disease is tauopathy.