ArticleAnnals of Indian Academy of Neurology2026
Exploring the Role of Nuclear Factor Kappa B in the Immunobiology of Inflammatory Neuropathies.
Article in Annals of Indian Academy of Neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesGuillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are inflammatory conditions, representing prototype examples of immune-mediated disorders of the peripheral nervous system. Activation of the nuclear factor-κB (NF-κB) pathway is crucial for generating immune and inflammatory responses and creating an inflammatory milieu; however, this has not been studied in inflammatory neuropathies. We aimed to quantify the expression levels of two critical genes in the NF-κB pathway ( Nfkb1 and Nfkb2 ), together with a prototype inflammatory gene, Tnfα , in inflammatory neuropathies.
methodsForty-nine patients with inflammatory neuropathies (GBS = 38, CIDP = 11) were recruited prospectively from a single neurology unit. Gene expression levels of Nf κ b1 , Nf κ b2 , and Tnfα were quantified using quantitative real-time polymerase chain reaction.
resultsThere were significantly increased expression levels of Nf κ b1 in the inflammatory neuropathy group compared to healthy controls ( P = 0.001), GBS versus healthy controls ( P = 0.03), and CIDP versus healthy controls ( P = 0.003). There were no significant differences in the expression levels of Nf κ b2 and Tnfα genes between cases and controls. There was no correlation between the expression levels of these genes and the clinical severity scores.
conclusionsThe present study provides evidence for NF-κB pathway activation in inflammatory neuropathies, including both GBS and CIDP, suggesting that this spectrum of disorders may share a common central pathway for immune activation. Thus, the NF-κB pathway plays a critical role in the immunopathogenesis of inflammatory neuropathies; however, the molecular interacting partners within the immune system need to be studied to identify the differential immune trajectories in GBS and CIDP.
Indexed as
Identifiers
What OpenQuestion holds
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.