Evidence map›Paper›PMID 18653182›Full record

ArticleExperimental eye research2008

Inflammatory demyelination induces axonal injury and retinal ganglion cell apoptosis in experimental optic neuritis.

Kenneth S Shindler, Elvira Ventura, Mahasweta Dutt, Abdolmohamad Rostami

Abstract read
In one paragraph

Article in Experimental eye research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
3.6field-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

91 citing papers in PubMed, 154 citations in OpenAlex.

  1. Trial
  2. Changepoint analysis of longitudinal OCT in optic neuritis: Structural stabilization dynamics and clinical correlates.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  3. Antioxidants (Basel, Switzerland) · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. MOGJournal of neuroinflammation · 2025
    Review
  9. Complement updates in optic neuritis.Frontiers in neurology · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Cathepsin-B inhibitor CA-074 attenuates retinopathy and optic neuritis in experimental autoimmune encephalomyelitis induced in SJL/J mice.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Article
  17. Article
  18. Review
  19. Review
  20. Immunopathology of the optic nerve in multiple sclerosis.Clinical and experimental immunology · 2022
    Article

31 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 2 institutions in 1 country.

Kenneth S ShindlerDepartment of Ophthalmology, F.M. Kirby Center for Molecular Ophthalmology, University of Pennsylvania, Philadelphia, PA 19104-6100, United States. kenneth.shindler@uphs.upenn.edu
Elvira Ventura
Mahasweta Dutt
Abdolmohamad Rostami
Jefferson Hospital for Neuroscience · USUniversity of Pennsylvania · US

Funding

Prevention of Neuronal Damage in Optic NeuritisK08EY015098 · NEI · UNIVERSITY OF PENNSYLVANIA · PI SHINDLER, KENNETH S · 2004 to 2008
$883k
NEI NIH HHS EY015098NEI NIH HHS K08 EY015098
6 · The paper itself

Abstract

Optic neuritis is an inflammatory disease of the optic nerve that often occurs in patients with multiple sclerosis and leads to permanent visual loss mediated by retinal ganglion cell (RGC) damage. Optic neuritis occurs with high frequency in relapsing-remitting experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, with significant loss of RGCs. In the current study, mechanisms of RGC loss in this model were examined to determine whether inflammation-induced axonal injury mediates apoptotic death of RGCs. RGCs were retrogradely labeled by injection of fluorogold into superior colliculi of 6-7 week old female SJL/J mice. EAE was induced one week later by immunization with proteolipid protein peptide. Optic neuritis was detected by inflammatory cell infiltration on histological examination as early as 9 days after immunization, with peak incidence by day 12. Demyelination occurred 1-2 days after inflammation began. Loss of RGC axons was detected following demyelination, with significant axonal loss occurring by day 13 post-immunization. Axonal loss occurred prior to loss of RGC bodies at day 14. Apoptotic cells were also observed at day 14 in the ganglion cell layer of eyes with optic neuritis, but not in control eyes. Together these results suggest that inflammatory cell infiltration mediates demyelination and leads to direct axonal injury in this model of experimental optic neuritis. RGCs die by an apoptotic mechanism triggered by axonal injury. Potential neuroprotective therapies to prevent permanent RGC loss from optic neuritis will likely need to be initiated prior to axonal injury to preserve neuronal function.

Indexed as

ApoptosisAnimalsAxonsCell DeathDemyelinating DiseasesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalIn Situ Nick-End LabelingMiceMice, Inbred StrainsOptic NeuritisRetinal Ganglion Cells

Identifiers

PMID18653182
PMCPMC2564281
OpenAlexW1976987174

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.