We conclude that DL0410 ameliorates cognitive deficits in APP/PS1 transgenic mice by promoting synaptic transmission via activating the AKT/GSK-3β and MAPK/ERK signaling pathway and reducing neuronal loss.
In short, our findings provide the first evidence that CK might attenuate cognitive deficits and Aβ<sub>1-42</sub> deposition in the hippocampus via enhancing the expression of pSer9-GSK-3β and IDE.
We then highlight evidence suggesting that GSK3β influences hippocampal volume in MDD patients, and how this could assist with targeting more precise treatments particularly for cognitive deficits in patients with mood disorders.