It primarily activates PKCε and PKCδ (with a particular emphasis on PKCε) to exert neuroprotective effects in various neurological disease models, including AD [343, 344], MS [345, 346, 347], fragile X syndrome (FXS) [348, 349, 350], stroke [351, 352, 353, 354], traumatic brain injury (TBI) [355, 356, 357], and depression [358, 359, 360]. This evidence concerns the gene PRKCE and depressive symptom measurement.