Sopraespressione di S100B promuove comportamenti depressivi simili in ratti indotti da ictus modulando il percorso PI3K/AKT/NF-κB.

Post-stroke depression (PSD) is a common complication following a stroke, primarily characterized by low mood, cognitive sluggishness, and sleep disturbances. Currently, the precise pathogenic mechanisms underlying PSD remain elusive. Research indicates that S100B protein levels may serve as a specific biochemical marker of organic brain injury, with significantly elevated serum S100B levels noted in patients with ischemic stroke, depression, and schizophrenia. S100B facilitates apoptosis through various cellular signaling pathways and is implicated in inflammatory responses, thereby participating in the pathophysiology of numerous diseases. Nonetheless, the role of elevated S100B expression