Evidence map›Paper›PMID 12651618›Full record

ArticleThe American journal of pathology2003

Axonal injury heralds virus-induced demyelination.

Ikuo Tsunoda, Li-Qing Kuang, Jane E Libbey, Robert S Fujinami

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 11% 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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Contribution of Intravital Neuroimaging to Study Animal Models of Multiple Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  6. Neurodegeneration in multiple sclerosis.WIREs mechanisms of disease · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Autophagy in Multiple Sclerosis: Two Sides of the Same Coin.Frontiers in cellular neuroscience · 2020
    Review
  17. Review
  18. Article
  19. Article
  20. Article

15 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

4 authors at 1 institution in 1 country.

Ikuo TsunodaDepartment of Neurology, University of Utah School of Medicine, Salt Lake City, Utah 84132, USA.
Li-Qing Kuang
Jane E Libbey
Robert S Fujinami
University of Utah · US

Funding

VIRAL AND CELLULAR DETERMINANTS INVOLVED IN CNS DISEASER01NS034497 · NINDS · UNIVERSITY OF UTAH · PI FUJINAMI, ROBERT S · 1995 to 2004
$1.0M
NINDS NIH HHS 2 R01 NS34497NINDS NIH HHS R01 NS034497
6 · The paper itself

Abstract

Axonal pathology has been highlighted as a cause of neurological disability in multiple sclerosis. The Daniels (DA) strain of Theiler's murine encephalomyelitis virus infects the gray matter of the central nervous system of mice during the acute phase and persistently infects the white matter of the spinal cord during the chronic phase, leading to demyelination. This experimental infection has been used as an animal model for multiple sclerosis. The GDVII strain causes an acute fatal polioencephalomyelitis without demyelination. Injured axons were detected in normal appearing white matter at 1 week after infection with DA virus by immunohistochemistry using antibodies specific for neurofilament protein. The number of damaged axons increased throughout time. By 2 and 3 weeks after infection, injured axons were accompanied by parenchymal infiltration of Ricinus communis agglutinin I(+) microglia/macrophages, but never associated with perivascular T-cell infiltration or obvious demyelination until the chronic phase. GDVII virus infection resulted in severe axonal injury in normal appearing white matter at 1 week after infection, without the presence of macrophages, T cells, or viral antigen-positive cells. The distribution of axonal injury observed during the early phase corresponded to regions where subsequent demyelination occurs during the chronic phase. The results suggest that axonal injury might herald or trigger demyelination.

Indexed as

TheilovirusAnimalsAxonsCardiovirus InfectionsDemyelinating DiseasesDisease Models, AnimalFemaleHumansImage Processing, Computer-AssistedInflammationMiceMice, Inbred StrainsMicroscopy, FluorescenceMultiple Sclerosis

Identifiers

PMID12651618
PMCPMC1851221
OpenAlexW1963968756

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.