Effect of Sodium Benzoate as an Add-on Therapy on the Clinical and Cognitive Symptoms of Schizophrenia: A Case Series

Abstract

Schizophrenia is understood as a construct of positive, negative, and cognitive symptoms. There has been considerable proof at a genetic, biochemical, and pharmacological level to support that N-methyl-D-aspartate Receptor (NMDAR) hypofunction is a key factor in the development of clinical and cognitive symptoms of schizophrenia. While most antipsychotics improve positive symptoms of schizophrenia, the negative and cognitive symptoms have usually been much more difficult to treat and have been associated with poor prognosis, poor functional outcome, and long-term morbidity. Sodium benzoate is a molecule that targets D-amino Acid Oxidase (DAAO) and competitively inhibits it, thus acting as an NMDAR agonist. With this background, we started using sodium benzoate as an adjuvant along with the ongoing antipsychotics in certain patients with schizophrenia to observe the change in clinical and cognitive symptoms. The authors have compiled a case series of 12 such patients. They found an improvement ranging from 17% to 21.5% in the Positive and Negative Syndrome Scale (PANSS) score and 19% to 32.5% in the Mini-mental State Examination (MMSE) Score after six weeks of administration of sodium benzoate as an add-on agent. None of the patients reported any adverse effects after six weeks. Thus, sodium benzoate as an add-on treatment can act as a neurocognitive enhancer as well as a novel antipsychotic that can bridge the gap in the treatment of schizophrenia.

Keywords

• antipsychotics
• cognition
• d amino acid oxidase