Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6271941 | Neuroscience | 2015 | 14 Pages |
Abstract
Psychiatric disorders, including major depressive disorder (MDD), bipolar disorder (BD) and schizophrenia, affect a significant percentage of the world population. These disorders are associated with educational difficulties, decreased productivity and reduced quality of life, but their underlying pathophysiological mechanisms are not fully elucidated. Recently, studies have suggested that psychiatric disorders could be considered as inflammatory disorders, even though the exact mechanisms underlying this association are not known. An increase in inflammatory response and oxidative stress may lead to inflammation, which in turn can stimulate microglia in the brain. Microglial activation is roused by the M1 phenotype, which is associated with an increase in interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). On the contrary, M2 phenotype is associated with a release of anti-inflammatory cytokines. Thus, it is possible that the inflammatory response from microglial activation can contribute to brain pathology, as well as influence treatment responses. This review will highlight the role of inflammation in the pathophysiology of psychiatric disorders, such as MDD, BD, schizophrenia, and autism. More specifically, the role of microglial activation and associated molecular cascades will also be discussed as a means by which these neuroinflammatory mechanisms take place, when appropriate.
Keywords
IFN-γadrenalectomizedTGF-βTh2Th1VPAP2X7RQUINIDOSSRIsHDACiADXN-methyl-d-aspartateNMDAIL-1βHspiNOSDAMPsMDDLPST-helper 1T-helper 2TLRspost-traumatic stress disorderPTSDMajor depressive disorderbipolar disorderautism spectrum disordersSchizophreniaQuinolinic acidNeuroinflammationdamage-associated molecular patternsAutisminterferon-γInterleukin-1βIndoleamine 2,3 dioxygenaselearned helplessnesstransforming growth factor-βTail suspensiontumor necrosis factor-αPositron emission tomographyValproateinducible nitric oxide synthaseForced swimmingTNF-αlipopolysaccharideCSFCerebrospinal fluidselective serotonin reuptake inhibitorshistone deacetylase inhibitorMicrogliaASDNitric oxidePETHeat shock proteinToll-like receptors
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Authors
G.Z. Réus, G.R. Fries, L. Stertz, M. Badawy, I.C. Passos, T. Barichello, F. Kapczinski, J. Quevedo,