PPARγ activation by troglitazone and rosiglitazone protected rat hippocampal neurons in culture against toxicity through exposure to synthetic Aβ1–40 peptide (5 μM), resulting in the modulation of Wnt signalling components, including the increase of the cytoplasmic and nuclear β-catenin levels and the inhibition of glycogen synthase kinase-3β (GSK-3β), suggesting that GSK-3β is responsible for the tau hyperphosphorylation in AD [75]. This evidence concerns the gene PPARG and Alzheimer disease.