Figure 1.

Involvement of GSK-3β in AD results from many activities. The most significant are reported in this figure. GSK-3β contributes to amyloid deposition production affecting the function of presenilin 1 (PS1) and the enzymatic cleavage of APP mediated by BACE-1; senile plaques are derived from the abnormal extracellular accumulation and deposition of Aβ peptide. GSK-3β is responsible for the hyperphosphorylation of tau protein and, as consequence, NFTs formation. GSK-3β is involved in neuroinflammation promoting the production of cytokines in astrocytes and microglia.