Superoxide dismutase, BDNF and cognitive improvement in drug-naive first episode patients with schizophrenia: a 12-week longitudinal study
Abstract Objective Cognitive improvement after antipsychotic agents in patients with schizophrenia (SCZ) appears to involve redox regulation through neurotrophins such as brain derived neurotropic factor (BDNF). This study examined whether cognitive improvement was associated with the increase in superoxide dismutase (SOD), and whether higher levels of BDNF could have a permissive role in allowing SOD to improve cognition. Methods We examined this hypothesis in 183 drug-naïve first episode (DNFE) SCZ patients taking risperidone monotherapy for 12 weeks. We measured total copper-zinc superoxide dismutase (CuZn-SOD), manganese superoxide dismutase (Mn-SOD) and SOD activities and BDNF levels in these patients and compared their levels to 152 healthy controls. We assessed cognitive functioning and clinical symptoms at baseline and 12-week follow-up. Results After treatment with risperidone, CuZn-SOD activity was significantly increased, and BDNF levels were slightly increased. Increased CuZn-SOD activity was associated with the cognitive effectiveness of risperidone monotherapy. The BDNF levels and SOD activities were correlated at baseline, but not correlated after 12-week treatment. Furthermore, baseline CuZn-SOD activity positively correlated with improvement on the delayed memory subscale of the RBANS only in high BDNF subgroup. Conclusions Our longitudinal study suggests that risperidone can enhance SOD activity and that in combination with higher baseline BDNF levels acting in a permissive role can improve cognitive impairments in SCZ. Greater baseline CuZn-SOD activity also may have predictive value for cognitive improvement of delayed memory in SCZ patients getting risperidone treatment.