A new pathophysiological aspect of S100B in schizophrenia: potential regulation of S100B by its scavenger soluble RAGE.

BACKGROUND

Several studies have reported elevated S100B serum levels in schizophrenia. Our study focused on its scavenger, soluble receptor for advanced glycation end products (sRAGE). Given the benefits of sRAGE in metabolic and inflammatory diseases, we hypothesized a similar effect in schizophrenia.

METHODS

S100B and sRAGE concentrations were explored during acute paranoid schizophrenia and during reconvalescence. Serum samples from 26 inpatients were investigated on hospital admission (T0) and 6 weeks posttreatment (T6) by S100B-immunoluminometry and sRAGE-ELISA. Thirty-two matched healthy individuals served as controls. Psychopathology was monitored using the Positive and Negative Syndrome Scale (PANSS).

RESULTS

S100B (p = .021) and sRAGE (p = .020) were elevated in schizophrenic patients at T0. S100B levels normalized under antipsychotic treatment (p = .003), whereas sRAGE increased further by T6 (p = .005). Changes of S100B during treatment correlated inversely with DeltasRAGE (r = -.422, p = .032). PANSS was negatively associated with sRAGE at T0 (positive score: r = -.415, p = .035; total score: r = -.395, p = .046).

CONCLUSIONS

Our results provide support for a reduction of S100B levels during reconvalescence from acute paranoid schizophrenia that is regulated by its scavenger sRAGE. This mechanism could provide novel treatment strategies.