ArticleFrontiers in psychiatry2011
Aberrant NF-kappaB expression in autism spectrum condition: a mechanism for neuroinflammation.
Article in Frontiers in psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
75 citing papers in PubMed, 3 syntheses or guidelines pooled it, 144 citations in OpenAlex.
- Postmortem Studies of Neuroinflammation in Autism Spectrum Disorder: a Systematic Review.Molecular neurobiology · 2020Pooled it
- Decreased Brain pH as a Shared Endophenotype of Psychiatric Disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Pooled it
- Acupuncture for autism spectrum disorders (ASD).The Cochrane database of systematic reviews · 2011Pooled it
- Evaluating the therapeutic efficacy of a modified ketogenic diet in children with autism spectrum disorder: a randomized controlled trial.BMC pediatrics · 2026Trial
- Mapping lncRNAs onto multilevel mRNA co‑expression modules in autism.Translational psychiatry · 2026Article
- Oxytocin and RAGE signaling at the intersection of social neurodevelopment and inflammation.Journal of translational medicine · 2026Review
- Microglia as critical mediators linking perinatal immune stress to mental health trajectories.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Early-life oxidative stress programs persistent NFκB activation and neuroinflammation in autism spectrum disorder.Frontiers in immunology · 2026Article
- Neuroinflammation and autism: what have we learned so far?International journal of developmental disabilities · 2026Article
- Valproate-Induced Autism and Sexual Hormone Disturbances: A Literature Review and Hypotheses.Neurochemical research · 2025Review
- Article
- Human Blood-Derived lncRNAs in Autism Spectrum Disorder.Biomolecules · 2025Review
- Prenatal inflammation impairs early CD11c-positive microglia induction and delays myelination in neurodevelopmental disorders.Communications biology · 2025Article
- Comparative effect of atorvastatin and risperidone on modulation of TLR4/NF-κB/NOX-2 in a rat model of valproic acid-induced autism.Behavioral and brain functions : BBF · 2024Article
- Targeting Microglia in Neuroinflammation: H3 Receptor Antagonists as a Novel Therapeutic Approach for Alzheimer's Disease, Parkinson's Disease, and Autism Spectrum Disorder.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Central Causation of Autism/ASDs via Excessive [CaBrain sciences · 2024Review
- Article
- Taurine as a potential therapeutic agent interacting with multiple signaling pathways implicated in autism spectrum disorder (ASD): An in-silico analysis.IBRO neuroscience reports · 2023Article
- Preclinical Evidence for the Role of the Yin/Yang Angiotensin System Components in Autism Spectrum Disorder: A Therapeutic Target of Astaxanthin.Biomedicines · 2023Article
- Microbiota-indole 3-propionic acid-brain axis mediates abnormal synaptic pruning of hippocampal microglia and susceptibility to ASD in IUGR offspring.Microbiome · 2023Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Autism spectrum condition (ASC) is recognized as having an inflammatory component. Post-mortem brain samples from patients with ASC display neuroglial activation and inflammatory markers in cerebrospinal fluid, although little is known about the underlying molecular mechanisms. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a protein found in almost all cell types and mediates regulation of immune response by inducing the expression of inflammatory cytokines and chemokines, establishing a feedback mechanism that can produce chronic or excessive inflammation. This article describes immunodetection and immunofluorescence measurements of NF-κB in human post-mortem samples of orbitofrontal cortex tissue donated to two independent centers: London Brain Bank, Kings College London, UK (ASC: n = 3, controls: n = 4) and Autism Tissue Program, Harvard Brain Bank, USA (ASC: n = 6, controls: n = 5). The hypothesis was that concentrations of NF-κB would be elevated, especially in activated microglia in ASC, and pH would be concomitantly reduced (i.e., acidification). Neurons, astrocytes, and microglia all demonstrated increased extranuclear and nuclear translocated NF-κB p65 expression in brain tissue from ASC donors relative to samples from matched controls. These between-groups differences were increased in astrocytes and microglia relative to neurons, but particularly pronounced for highly mature microglia. Measurement of pH in homogenized samples demonstrated a 0.98-unit difference in means and a strong (F = 98.3; p = 0.00018) linear relationship to the expression of nuclear translocated NF-κB in mature microglia. Acridine orange staining localized pH reductions to lysosomal compartments. In summary, NF-κB is aberrantly expressed in orbitofrontal cortex in patients with ASC, as part of a putative molecular cascade leading to inflammation, especially of resident immune cells in brain regions associated with the behavioral and clinical symptoms of ASC.
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Registered trials
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.