Redox and Immune Signaling in Schizophrenia: New Therapeutic Potential

dc.contributor.authorDwir, Daniellaen
dc.contributor.authorKhadimallah, Inesen
dc.contributor.authorXin, Lijingen
dc.contributor.authorRahman, Meredithen
dc.contributor.authorDu, Feien
dc.contributor.authorOngur, Dosten
dc.contributor.authorDo, Kim Q.en
dc.date.accessioned2023-09-29T13:28:46Zen
dc.date.available2023-09-29T13:28:46Zen
dc.date.issued2023-05en
dc.description.abstractRedox biology and immune signaling play major roles in the body, including in brain function. A rapidly growing literature also suggests that redox and immune abnormalities are implicated in neuropsychiatric conditions such as schizophrenia (SZ), bipolar disorder, autism, and epilepsy. In this article we review this literature, its implications for the pathophysiology of SZ, and the potential for development of novel treatment interventions targeting redox and immune signaling. Redox biology and immune signaling in the brain are complex and not fully understood; in addition, there are discrepancies in the literature, especially in patient-oriented studies. Nevertheless, it is clear that abnormalities arise in SZ from an interaction between genetic and environmental factors during sensitive periods of brain development, and these abnormalities disrupt local circuits and long-range connectivity. Interventions that correct these abnormalities may be effective in normalizing brain function in psychotic disorders, especially in early phases of illness.en
dc.description.notesWe thank National Center of Competence in Research (NCCR) "SYNAPSY - The Synaptic Bases of Mental Diseases" from the Swiss National Science Foundation (no. 51AU40_185897 to K.Q.D.), the Istanjac Foundation (PIs: I.K., L.X.), and the Alamaya Foundation (PI: I.K.) as well as R01MH114982 to D.O./F.D. and P50MH115846 to D.O. D.D. is funded by the Adrian and Simone Frutiger Foundation (PI: D.D.).en
dc.description.sponsorshipNational Center of Competence in Research (NCCR) "SYNAPSY - The Synaptic Bases of Mental Diseases" from the Swiss National Science Foundation [51AU40_185897]; Istanjac Foundation; Alamaya Foundation [R01MH114982, P50MH115846]; Adrian and Simone Frutiger Foundationen
dc.description.versionPublished versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.1093/ijnp/pyad012en
dc.identifier.eissn1469-5111en
dc.identifier.issn1461-1457en
dc.identifier.issue5en
dc.identifier.pmid36975001en
dc.identifier.urihttp://hdl.handle.net/10919/116371en
dc.identifier.volume26en
dc.language.isoenen
dc.publisherOxford University Pressen
dc.rightsCreative Commons Attribution-NonCommercial 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/en
dc.subjectOxidative stressen
dc.subjectneuro-inflammationen
dc.subjectparvalbumin neuronsen
dc.subjectschizophreniaen
dc.subjectglutathioneen
dc.subjectNADen
dc.subjectNADHen
dc.titleRedox and Immune Signaling in Schizophrenia: New Therapeutic Potentialen
dc.title.serialInternational Journal of Neuropsychopharmacologyen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten

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