S100B in schizophrenia: an update

Abstract

Recent research has supported a potential role of immune pathology in the etiopathogenesis of schizophrenic. In the CNS various viruses were identified in the brains of schizophrenic patients. Pro-inflammatory cytokines were found to be associated with the stage of disease. Microglial cells were reported to be activated in a subgroup of schizophrenic patients in post mortem as well as imaging studies. New research has demonstrated that astrocytes together with microglial cells are the major immunocompetent cells of the brain and play an important role in the regulation of neuronal proliferation and differentiation. S100B, a calcium binding astrocyte-specific cytokine, presents a marker of astrocytic activation. Scientific evidence for increased S100B in acute schizophrenia is very consistent. The picture is not as clear regarding schizophrenia subtypes in acute states but patients with persistent negative symptoms or deficit syndrome show constant high S100B concentrations. There is an association between high S100B and poor therapeutic response. The increased S100B concentrations appear to be functionally relevant since they are reflected by poor cognitive performance and cross validation with other methods make it unlikely that the findings are merely an epiphenomenon. These findings suggest that the activation of astrocytes might be an important pathogenic factor for the development of schizophrenia.