ArticleBiological psychiatry2019
The Role of the Nuclear Factor-κB Transcriptional Complex in Cortical Immune Activation in Schizophrenia.
Article in Biological psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 3 of them syntheses that pooled it.
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Who cites it
46 citing papers in PubMed, 3 syntheses or guidelines pooled it, 78 citations in OpenAlex.
- The impact of sex on gene expression in the brain of schizophrenic patients: a systematic review and meta-analysis of transcriptomic studies.Biology of sex differences · 2024Pooled it
- Brain Inflammatory Marker Abnormalities in Major Psychiatric Diseases: a Systematic Review of Postmortem Brain Studies.Molecular neurobiology · 2023Pooled it
- Immune System Abnormalities in Schizophrenia: An Integrative View and Translational Perspectives.Frontiers in psychiatry · 2022Pooled it
- The role ofEpigenetics · 2026Review
- Is increased inflammation in schizophrenia associated with increased cardiovascular risk and the etiopathogenesis of this disorder?Brain, behavior, & immunity - health · 2026Article
- Serum TLR4, NF-κB, and NLRP3 Levels in Children with Attention-Deficit/Hyperactivity Disorder: A Case-Control Study.Children (Basel, Switzerland) · 2026Article
- Myo-inositol concentration in the medial prefrontal cortex is associated with changes in brain white matter microstructure in early psychosis.Translational psychiatry · 2026Article
- Molecular mechanisms of olanzapine against agitation in schizophrenia and bipolar disorder based on network pharmacology and molecular docking.Scientific reports · 2025Article
- Cardiovascular protein profiling in patients with first-episode psychosis.Schizophrenia (Heidelberg, Germany) · 2025Article
- uN2CpolyG-mediated p65 nuclear sequestration suppresses the NF-κB-NLRP3 pathway in neuronal intranuclear inclusion disease.Cell communication and signaling : CCS · 2025Article
- First Description of the Role of the Relationship Between Serum Amyloid P Components and Nuclear Factors/Pro-Cytokines During Critical Periods of Toxoplasmic Encephalitis.Brain sciences · 2024Article
- A Selective Nuclear Factor-κB Inhibitor, JSH-23, Exhibits Antidepressant-like Effects and Reduces Brain Inflammation in Rats.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Massively parallel characterization of regulatory elements in the developing human cortex.Science (New York, N.Y.) · 2024Article
- Behavioral and transcriptional effects of repeated electroconvulsive seizures in the neonatal MK-801-treated rat model of schizophrenia.Psychopharmacology · 2024Article
- Immune and metabolic challenges induce changes in pain sensation and related pathways in the hypothalamus.Physiological genomics · 2024Article
- Toll-Like Receptor mRNA Levels in Schizophrenia: Association With Complement Factors and Cingulate Gyrus Cortical Thinning.Schizophrenia bulletin · 2024Article
- Acute IL-6 exposure triggers canonical IL6Ra signaling in hiPSC microglia, but not neural progenitor cells.Brain, behavior, and immunity · 2023Article
- Massively parallel characterization of psychiatric disorder-associated and cell-type-specific regulatory elements in the developing human cortex.bioRxiv : the preprint server for biology · 2023Article
- Review
- New insight in the cross-talk between microglia and schizophrenia: From the perspective of neurodevelopment.Frontiers in psychiatry · 2023Review
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5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTranscript levels for cytokines and the viral restriction factor interferon-induced transmembrane protein are markedly higher in the prefrontal cortex in schizophrenia. These gene products are regulated by the nuclear factor-κB (NF-κB) transcriptional complex. NF-κB activity, which requires the formation of NF-κB family member heterodimers, is regulated by activation receptors, kinases, and inhibitors. Whether any of these factors are altered in schizophrenia is not known. It is also unclear whether NF-κB-related disturbances reflect ongoing cortical immune activation or a long-lasting response to a prenatal immune-related insult.
methodsTranscript levels for NF-κB pathway markers were assessed using quantitative polymerase chain reaction in the prefrontal cortex from 1) 62 matched pairs of schizophrenia and unaffected comparison subjects, 2) antipsychotic-exposed monkeys, and 3) adult mice exposed prenatally to maternal immune activation or in adulthood to the immune stimulant polyinosinic-polycytidylic acid.
resultsIn schizophrenia subjects, but not antipsychotic-exposed monkeys, we found higher messenger RNA levels for 1) most NF-κB family members, 2) all NF-κB activation receptors, 3) several kinases, and 4) one inhibitor (IκBα) whose transcript level is itself regulated by NF-κB activity. A similar pattern of elevated NF-κB-related messenger RNA levels was seen in adult mice that received daily polyinosinic-polycytidylic acid injections, but not in adult mice subjected to maternal immune activation in utero.
conclusionsHigher NF-κB activity, evidenced by elevated transcript levels for NF-κB family members, activation receptors, and kinases, may contribute to increased markers of cortical immune activation in schizophrenia.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.