Evidence map›Paper›PMID 17823280›Full record

ArticleThe American journal of pathology2007

Targeting inflammatory demyelinating lesions to sites of Wallerian degeneration.

Ikuo Tsunoda, Tomoko Tanaka, Yukio Saijoh, Robert S Fujinami

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.9field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Animal models of Multiple Sclerosis.European journal of pharmacology · 2015
    Review
  9. The primate autoimmune encephalomyelitis model; a bridge between mouse and man.Annals of clinical and translational neurology · 2015
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Theiler's virus infection: Pathophysiology of demyelination and neurodegeneration.Pathophysiology : the official journal of the International Society for Pathophysiology · 2011
    Article
  16. Neuropathogenesis of Theiler's murine encephalomyelitis virus infection, an animal model for multiple sclerosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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 2 institutions in 2 countries.

Ikuo TsunodaDepartment of Neurology, University of Utah School of Medicine, Salt Lake City, UT 84132-2305, USA.
Tomoko Tanaka
Yukio Saijoh
Robert S Fujinami
University of Utah · USInstitute of Human Genetics · PL

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 NS34497NINDS NIH HHS R01 NS034497
6 · The paper itself

Abstract

In Theiler's murine encephalomyelitis virus (TMEV) infection, an animal model for multiple sclerosis (MS), axonal injury precedes inflammatory demyelinating lesions, and the distribution of axonal damage present during the early phase of infection corresponds to regions where subsequent demyelination occurs during the chronic phase. We hypothesized that axonal damage recruits inflammatory cells to sites of Wallerian degeneration, leading to demyelination. Three weeks after TMEV infection, axonal degeneration was induced in the posterior funiculus of mice by injecting the toxic lectin Ricinus communis agglutinin (RCA) I into the sciatic nerve. Neuropathology was examined 1 week after lectin injection. Control mice, infected with TMEV but receiving no RCA I, had inflammatory demyelinating lesions in the anterior/lateral funiculi. Other control mice that received RCA I alone did not develop inflammatory lesions. In contrast, RCA I injection into TMEV-infected mice induced lesions in the posterior funiculus in addition to the anterior/lateral funiculi. We found no differences in lymphoproliferative responses or antibody titers against TMEV among the groups. This suggests that axonal degeneration contributes to the recruitment of inflammatory cells into the central nervous system by altering the local microenvironment. In this scenario, lesions develop from the axon (inside) to the myelin (outside) (Inside-Out model).

Indexed as

AnimalsAntibodies, ViralAxonsCell LineCricetinaeDisease Models, AnimalFemaleGanglia, SpinalMiceMultiple SclerosisMyelin SheathPlant LectinsSciatic NerveTheilovirusWallerian DegenerationAntibodies, ViralPlant LectinsRicinus communis agglutinin-1

Identifiers

PMID17823280
PMCPMC2043517
OpenAlexW1981914856

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.