Targeting of inflammation and prostaglandins by nonsteroidal anti-inflammatory drugs in schizophrenia: A narrative review.

Schizophrenia is a neuropsychiatric disease characterized by psychotic symptoms. The mesolimibic system's exaggeration of dopaminergic and reduction of glutamatergic neurotransmissions contribute to the pathophysiology of schizophrenia. Antipsychotic drugs are a mainstay in the management of schizophrenia, though 30 % of schizophrenic cases do not respond to the effects of antipsychotics. In addition, first-generation antipsychotic drugs such as haloperidol are associated with serious adverse effects such as tardive dyskinesia and malignant hyperthermia syndrome. Likewise, second-generation antipsychotic drugs such as olanzepin increase the risk for the development of metabolic syndrome, obesity, and type 2 diabetes (T2D). Moreover, the pathogenesis of schizophrenia implicates chronic inflammatory conditions and the upregulation of cyclooxygenase (COX) enzymes. Therefore, targeting inflammation, specifically COX enzymes and the prostaglandin generated by non-steroidal anti-inflammatory drugs (NSAIDs), could potentially aid in the treatment of schizophrenia. Therefore, this review aims to explore the connection between inflammation, COX expression, and the pathogenesis of schizophrenia, as well as the potential effectiveness of NSAIDs in managing this mental disorder. This review conducted a search of electronic databases to identify the relationship between chronic inflammation and schizophrenia, focusing on the roles of COX, prostaglandin, and NSAIDs. In conclusion, NSAIDs could be an effective adjuvant therapeutic strategy in treating schizophrenia by targeting different pathways, including brain COX and the neuroinflammatory signaling pathway. Therefore, repurposing NSAIDs as add-on antipsychotic drugs may be effective in managing schizophrenia.