Neuroinflammation and Microglial Activation in Schizophrenia: An Overview

Schizophrenia has been classified recently to be initiated as a neuroinflammatory disorder that may upgrade later into neurodegenerative one. There are many clinical evidence which point to neuroinflammation in schizophrenia, and there are also many research works which highlight the elevation of pro-inflammatory cytokines such as IL-2 and IL-6 and the reduction of anti-inflammatory cytokines levels such as IL-4 and IL-10 in the schizophrenic patients. Cytokines are not only the key inflammatory players that have been discovered in correlation with schizophrenia; there are also other critical factors that are involved in the neuroinflammatory state in this disorder, which are the microglia and its activation. Microglia is one of the important players in the neuroinflammation in schizophrenia. It is well-known now that microglia is activated by number of cytokines that may be resulted from infection and/or stress, and microglial activation also has been strongly linked to kynurenine pathway, a neuroinflammatory pathway involved in schizophrenia. This pathway is documented to cause massive neurotoxicity and, thus, neurodegeneration in many neurological disorders such as AD, PD, and ALS and has been recently involved in schizophrenia. Moreover, translocator protein (TSPO), which is expressed in CNS glial cells as microglia, is considered in many studies as a good biomarker and potential therapeutic target in many neuroinflammatory disorders. Scientists studied the effect of using anti-inflammatory drugs in treating schizophrenia and found promising results.