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The Role of Cytokines in the Pathophysiology of Schizophrenia

Kyoung-Sae Na

Gachon University Gil Medical Center, Korea

Background/Objective: Schizophrenia is a chronic and debilitating mental disorder. The negative
and cognitive symptoms of schizophrenia are persistent and unresponsive to pharmacotherapy, which
indicates neurodegenerative aspects of schizophrenia. Dysregulation of neuroinflammation and
neurogenesis mechanisms greatly contribute to the neurodegeneration of schizophrenia.Cytokines are
pleiotropic glycoproteins produced by both peripheral immunocompetent cells and glial cells in the
CNS. In this narrative review, the role of cytokines for the pathophysiology of schizophrenia is
thoroughly discussed.

Method: Literature searches of five major electronic databases, including Medline, Embase,
Cochrane Library of Systematic Reviews, and PsycINFO, were conducted

Result: Current evidences suggest that, unlike peripheral inflammatory responses,
neuroinflammation plays roles in a number of neuronal activities such as neurogenesis and
neuroplasticity. Cross-talk between neuroinflammation and neurogenesis is usually beneficial for the
CNS under physiological conditions. Cytokines can cross blood-brain barrier by various mechanisms.
In the CNS, cytokines also involved in various neural interactions such as neurogenesis and synaptic
plasticity. Particularly, pro-inflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6
(IL-6), and tumor necrosis factor-α (TNF-α) mediate and facilitate neural activities as well as the
inflammatory process. Pro-inflammatory cytokine receptors are highly aggregated in regions with
cognitive function such as the hippocampus. The relative abundance of pro-inflammatory cytokines
in the hippocampus suggests that these pleiotropic molecules play a role in long-term potentiation,the
cellular basis of short-term memory, and glutamate-dependent synaptic plasticity. However,
uncontrolled and chronic neuroinflammation mediated by pro-inflammatory cytokines has
detrimental effects such as neuronal loss, inhibition of neurogenesis, and excessive oxidative stress.
Particularly, neuroinflammation and pro-inflammatory cytokines influence on the kynurenine
pathway, consequently contribute to the pathophysiology of schizophrenia.

Conclusion: Our findings suggest that electroconvulsive shock improves schizophrenia-like
behavior in Gunn rat, and attenuates microglial and astrocytes activation in the hippocampal of Gunn
rat. Which shows that important way of ECS works are through the role of neuroinflammation and
the immune system.