Cognitive improvement following antipsychotic drugs appears to require redox modulation via neurotrophins such as a brain-derived neurotrophic factor in people with schizophrenia (SCZ) (BDNF). For a study, researchers sought to analyze if cognitive enhancement was linked to an increase in superoxide dismutase (SOD) and if greater levels of BDNF played a role in allowing SOD to improve cognition.
The idea was tested in 183 drug-free first-episode patients with SCZ who received risperidone monotherapy for 12 weeks. Total copper-zinc SOD (CuZn-SOD), manganese SOD (Mn-SOD), and SOD activity, as well as BDNF levels, were assessed in the patients and compared to 152 healthy controls. At baseline and during a 12-week follow-up, they measured cognitive functioning and clinical symptoms.
The cuZn-SOD activity was dramatically raised after risperidone administration, but BDNF levels were modestly elevated. Increased CuZn-SOD activity was linked to risperidone monotherapy’s cognitive efficacy. At baseline, BDNF levels and SOD activity were associated, but not after a 12-week therapy. Furthermore, only in the high BDNF category did baseline CuZn-SOD activity correspond with improvement on the delayed memory subscale of the Repeatable Battery for the Assessment of Neuropsychological Status.
The longitudinal investigation demonstrated that risperidone could alleviate cognitive deficits in SCZ by increasing SOD activity and when combined with greater baseline BDNF levels operating in a permissive role. Greater baseline CuZn-SOD activity might also be indicative of cognitive improvement in SCZ patients undergoing risperidone therapy.