Evidence map›Paper›PMID 17924980›Full record

ArticleBrain pathology (Zurich, Switzerland)2008

Glutamate receptor expression in multiple sclerosis lesions.

Jia Newcombe, Alim Uddin, Rosamund Dove, Bela Patel, Lechoslaw Turski, Yukio Nishizawa, Terence Smith

Open access · greenAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

74 citing papers in PubMed, 161 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Observational
  7. Article
  8. Article
  9. Synapse Dysfunctions in Multiple Sclerosis.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. RNA aptamers for AMPA receptors.Neuropharmacology · 2021
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

14 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Jia NewcombeDepartment of Neuroinflammation, Institute of Neurology, University College London, London, UK. J.Newcombe@ion.ucl.ac.uk
Alim Uddin
Rosamund Dove
Bela Patel
Lechoslaw Turski
Yukio Nishizawa
Terence Smith
Eisai (United Kingdom) · GBUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blockade of receptors for the excitatory neurotransmitter glutamate ameliorates neurological clinical signs in models of the CNS inflammatory demyelinating disease multiple sclerosis (MS). To investigate whether glutamate excitoxicity may play a role in MS pathogenesis, the cellular localization of glutamate and its receptors, transporters and enzymes was examined. Expression of glutamate receptor (GluR) 1, a Ca(++)-permeable ionotropic AMPA receptor subunit, was up-regulated on oligodendrocytes in active MS lesion borders, but Ca(++)-impermeable AMPA GluR2 subunit levels were not increased. Reactive astrocytes in active plaques expressed AMPA GluR3 and metabotropic mGluR1, 2/3 and 5 receptors and the GLT-1 transporter, and a subpopulation was immunostained with glutamate antibodies. Activated microglia and macrophages were immunopositive for GluR2, GluR4 and NMDA receptor subunit 1. Kainate receptor GluR5-7 immunostaining showed endothelial cells and dystrophic axons. Astrocyte and macrophage populations expressed glutamate metabolizing enzymes and unexpectedly the EAAC1 transporter, which may play a role in glutamate uptake in lesions. Thus, reactive astrocytes in MS white matter lesions are equipped for a protective role in sequestering and metabolizing extracellular glutamate. However, they may be unable to maintain glutamate at levels low enough to protect oligodendrocytes rendered vulnerable to excitotoxic damage because of GluR1 up-regulation.

Indexed as

AdultAgedAged, 80 and overAstrocytesCentral Nervous SystemExcitatory Amino Acid Transporter 3FemaleGliosisGlutamic AcidHumansKainic Acid ReceptorsMacrophagesMaleMiddle AgedMultiple SclerosisNerve Fibers, MyelinatedExcitatory Amino Acid Transporter 3Glutamic AcidKainic Acid ReceptorsNeurotoxinsProtein SubunitsReceptors, AMPASLC1A1 protein, humanVesicular Glutamate Transport Proteins

Identifiers

PMID17924980
PMCPMC8095601
OpenAlexW2012682323

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.