Abstract

A better understanding of the key molecules/pathways underlying the pathophysiology of depression and schizophrenia may contribute to novel therapeutic strategies. In this review, we have discussed the recent developments on the role of inflammatory pathways in the pathogenesis of depression and schizophrenia. Inflammation is an innate immune response that can be triggered by various factors, including pathogens, stress and injury. Under normal conditions, the inflammatory responses quiet after pathogen clearance and tissue repair. However, abnormal long-term or chronic inflammation can lead to damaging effects. Accumulating evidence suggest that dysregulated inflammation is linked to the pathogenesis of neuropsychiatric disorders. In this review, we have discussed the roles of complement system, infiltration of peripheral immune cells into the central nervous system (CNS), the gut-brain axis, and the kynurenine pathway in depression and schizophrenia. There is a large body of compelling evidence on the role of inflammatory pathways in depression and schizophrenia. Although most of these findings show their roles in the pathophysiology of the above disorders, additional studies are warranted to investigate the therapeutic potential of various immune signaling targets discussed in this article.

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