GSK-3β regulates Aβ production affecting the functionof presenilin 1 (PS1),91 a component ofthe γ-secretase complex, and the enzymatic cleavage of APP mediatedby BACE-1.92 Furthermore, NF-κB,overexpressed in AD patients, mediates GSK-3β-induced BACE-1expression.93 To complete this loop, ithas been observed that Aβ blocks Wnt-mediated GSK-3β-inhibitionleading to an increase in Aβ formation and tau hyperphosphorylation.94 The gene discussed is APP; the disease is Alzheimer disease.