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Extracellular S100B dramatically increases after brain injury. While low S100B levels are neuroprotective, micromolar S100B levels have shown in vitro to activate microglia and facilitate neuronal death. In astrocytes, S100B exposure activates nuclear factor kappa B (NF‐κB) and induces pro‐inflammatory mediators. On microglia and neurons S100B effects are essentially mediated by receptor for advanced...