Introduction

Schizophrenia is a complex psychiatric disorder characterized by disturbances in thought, perception, and cognition, traditionally explained through dopaminergic and glutamatergic hypotheses. However, recent research has highlighted the critical role of neuroinflammation in its pathophysiology, linking immune system dysregulation, microglial activation, and pro-inflammatory cytokine signaling to altered brain function. This emerging paradigm suggests that schizophrenia may not solely be a neurotransmitter imbalance but a disorder with significant immunological underpinnings, opening avenues for novel diagnostic and therapeutic approaches [1].

Description

Neuroinflammation in schizophrenia has been increasingly supported by evidence of elevated pro-inflammatory cytokines such as interleukin-6, interleukin-1β, and tumor necrosis factor-α in the peripheral blood and cerebrospinal fluid of patients. Postmortem studies have shown activated microglia, the brainâ??s resident immune cells, which may contribute to synaptic pruning abnormalities, altered neuroplasticity, and white matter dysfunction. These immune disturbances are thought to interact with genetic susceptibility, prenatal infections, and environmental stressors, thereby increasing vulnerability to the disorder [2].

Importantly, inflammatory pathways may converge with classical neurotransmitter systems, explaining clinical heterogeneity and treatment resistance. Beyond pathophysiology, neuroinflammatory markers are being explored as potential biomarkers for diagnosis, prognosis, and treatment monitoring For example, C-Reactive Protein (CRP) and cytokine profiles have been correlated with symptom severity and cognitive decline in schizophrenia highlighting [3].

Their utility in precision medicine approaches. Neuroimaging studies using Positron Emission Tomography (PET) tracers to detect microglial activation further support the role of inflammation in disease progression. Such tools not only enhance understanding of underlying mechanisms but also provide potential for early identification of at-risk individuals and stratification of patients based on inflammatory status. Therapeutically, targeting neuroinflammation has opened new horizons in schizophrenia treatment [4].

Anti-inflammatory agents such as Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), minocycline, and omega-3 fatty acids have shown modest benefits as adjunctive therapies, particularly in alleviating negative symptoms and cognitive deficits. More advanced strategies, including monoclonal antibodies against pro-inflammatory cytokines and immune-modulatory agents, are under clinical investigation [5].

Conclusion

The recognition of neuroinflammation as a key contributor to schizophrenia pathophysiology marks a significant advancement in psychiatric research. By bridging immune dysregulation with neural dysfunction, this perspective expands our understanding beyond neurotransmitter models and underscores the potential for immunomodulatory therapies. Continued research into inflammatory biomarkers and targeted treatments holds promise for more personalized, effective, and holistic management of schizophrenia, offering hope for better outcomes in this challenging disorder.

Acknowledgment

None.

Conflict of Interest

None.

References

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