Evidence map›Paper›PMID 22915098›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Nuclear factor κB activation impairs ependymal ciliogenesis and links neuroinflammation to hydrocephalus formation.

Michael Lattke, Alexander Magnutzki, Paul Walther, Thomas Wirth, Bernd Baumann

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
1.9field-weighted citation impact, top 16% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Frontiers in genetics · 2026
    Article
  5. Serum Biomarkers in Paediatric Neurosurgery: Traumatic Brain Injury and Beyond.Advances and technical standards in neurosurgery · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Genetic and molecular mechanisms of hydrocephalus.Frontiers in molecular neuroscience · 2024
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Novel therapeutic modulators of astrocytes for hydrocephalus.Frontiers in molecular neuroscience · 2022
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Michael LattkeInstitute of Physiological Chemistry, Ulm University, 89081 Ulm, Germany.
Alexander Magnutzki
Paul Walther
Thomas Wirth
Bernd Baumann
Physiological Society · GBUniversität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hydrocephalus formation is a frequent complication of neuropathological insults associated with neuroinflammation. However, the mechanistic role of neuroinflammation in hydrocephalus development is unclear. We have investigated the function of the proinflammatory acting inhibitor of κB kinase (IKK)/nuclear factor κB (NF-κB) signaling system in neuroinflammatory processes and generated a novel mouse model that allows conditional activation of the IKK/NF-κB system in astrocytes. Remarkably, NF-κB activation in astrocytes during early postnatal life results in hydrocephalus formation and additional defects in brain development. NF-κB activation causes global neuroinflammation characterized by a strong, astrocyte-specific expression of proinflammatory NF-κB target genes as well as a massive infiltration and activation of macrophages. In this animal model, hydrocephalus formation is specifically induced during a critical time period of early postnatal development, in which IKK/NF-κB-induced neuroinflammation interferes with ependymal ciliogenesis. Our findings demonstrate for the first time that IKK/NF-κB activation is sufficient to induce hydrocephalus formation and provides a potential mechanistic explanation for the frequent association of neuroinflammation and hydrocephalus formation during brain development, namely impairment of ependymal cilia formation. Therefore, our study might open up new perspectives for the treatment of certain types of neonatal and childhood hydrocephalus associated with hemorrhages and infections.

Indexed as

HydrocephalusAge FactorsAnimalsAnimals, NewbornAstrocytesBrainCell Adhesion MoleculesCells, CulturedCerebral CortexChemokinesComplement System ProteinsDisease Models, AnimalDoxycyclineEncephalitisEnzyme ActivationGene Expression Regulation, DevelopmentalCell Adhesion MoleculesChemokinesComplement System ProteinsDoxycyclineGlial Fibrillary Acidic ProteinI-kappa B KinaseI-kappa B ProteinsIkbkb protein, mouseNF-kappaB-Inducing KinaseNF-KappaB Inhibitor alphaNFKBIA protein, humanNfkbia protein, mouseProtein Serine-Threonine KinasesRela protein, mouseTranscription Factor RelA

Identifiers

PMID22915098
PMCPMC6703776
OpenAlexW2026279664

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.