Neuroinflammation and oxidative stress in schizophrenia: are these opportunities for repurposing?

Purpose: To summarize the main findings on the subject of neuroinflammation and oxidative stress in patients with Schizophrenia (SCZ). Methods: A narrative review of all the relevant papers known to the authors was conducted. Results: SCZ is a chronic, debilitating, neuropsychiatric disorder associated with an immense and adverse impact on both the patient and the caregiver, and impairs the overall quality of life. The current modality of treatment involves the use of antipsychotics to balance the disturbances in the neurotransmitters in the dopaminergic and serotonin pathways in the brain, which have a role to play in SCZ. Contemporary management of SCZ focuses mainly on symptomatic control due to the lack of effective curative treatments.Despite the optimum use of antipsychotics, there is a considerable proportion of the patient population who are poor responders. This has necessitated the exploration of new etiopathologies in order to evolve new modalities of treatment. This narrative review, conducted over a period of 3 months, throws light on the large-scale evidence pointing toward neuroinflammation and oxidative stress as key etiopathological markers that merit further consideration in SCZ, and may even be the basis for devising novel pharmacotherapies for SCZ. Conclusions: This review discusses the various plausible hypotheses, viz., cytokine hypothesis of peripheral inflammation, acute-phase reactants in SCZ, microglial hypothesis of central inflammation, neurogenesis in relation to neuroinflammation, and oxidative stress in SCZ. It also highlights the many opportunities available for repurposing already marketed drugs with anti-inflammatory and antioxidant properties with a view to devising more effective and comprehensive therapies to manage SCZ.

Automated summary

This narrative review summarizes the main findings on neuroinflammation and oxidative stress in patients with Schizophrenia, highlighting them as potential key etiopathological markers for the disease and suggesting opportunities for developing novel pharmacotherapies.