GSK3B and Alzheimer disease: The present data revealed that FLX significantly inhibited GSK-3β activity, increased the p-GSK-3β/GSK-3β ratio and stabilized the β-catenin level in vivo, indicating that activation of the Wnt signaling pathway might be involved in the neuroprotective effects of FLX that prevent neuronal loss in AD, as has been proposed for the in vitro neuroprotective effects [49].