Cognitive dysfunction correlates with elevated serum S100B concentration in drug-free acutely relapsed patients with schizophrenia.

Abstract

S100B, a biomarker of glial dysfunction and blood-brain barrier (BBB) disruption, has been proposed to be involved in the pathophysiology of schizophrenia. In the present study, we aimed at exploring the association of serum S100B levels with cognitive deficits using MATRICS Consensus Cognitive Battery (MCCB) in schizophrenia, by excluding the impact of antipsychotics. Sixty-two unmedicated patients with schizophrenia during their acute phases were divided into a drug-naïve group (n=34) and a drug-free group (n=28). S100B serum concentrations were measured and MCCB was administered to all of the patients. Forty healthy controls donated their blood samples for S100B assessment. The results indicated that serum S100B was significantly elevated in the drug-naive/free acute-stage schizophrenic patients when compared to the healthy controls. In the drug-free group, the serum S100B level was an independent contributor to the global cognitive dysfunctions, particularly for the speed of processing, attention/vigilance, visual learning and reasoning/problem solving subscores. Nevertheless, no significant associations between S100B and MCCB composite score or any cognitive domain subscore were observed in the drug-naïve group. These findings support the hypothesis that glial dysfunction and associated marker protein S100B may contribute to the pathophysiologic development of neurocognitive deficits in the relapsed individuals with schizophrenia.