Evidence map›Paper›PMID 17385943›Full record

ReviewDrugs2007

Pharmacological neuroprotection for glaucoma.

Glyn Chidlow, John P M Wood, Robert J Casson

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Drugs, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00739154 (Clinical Cohort Study of Association Between Steady State Phenytoin Treatment and Better Clinical Parameters of Glaucoma), which is not on this map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.2field-weighted citation impact, top 4% 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.

NCT00739154 unknown statusnot on this mapstarted 2008, after this paper: background citation

Clinical Cohort Study of Association Between Steady State Phenytoin Treatment and Better Clinical Parameters of Glaucoma

TypeobservationalSponsorRabin Medical CenterRan2008 to 2010Enrolled200ConditionsPrimary Open Angle Glaucoma, Secondary Open Angle Glaucoma, Narrow-Angle Glaucomas, Normal Tension Glaucoma
3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Glaucomatous optic neuropathy management: the role of neuroprotective agents.Medical hypothesis, discovery & innovation ophthalmology journal · 2013
    Review
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Glyn ChidlowOphthalmic Research Laboratories, South Australian Institute of Ophthalmology, Hanson Institute, Adelaide, South Australia, Australia. glyn.chidlow@imvs.sa.gov.au
John P M Wood
Robert J Casson
Hanson Institute · AUUniversity of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glaucoma represents a group of neurodegenerative diseases characterised by structural damage to the optic nerve and slow, progressive death of retinal ganglion cells (RGCs). Elevated intraocular pressure is traditionally considered to be the most important risk factor for glaucoma, and treatment options for the disease have hitherto been limited to its reduction. However, visual field loss and RGC death continue to occur in patients with well controlled intraocular pressures and, thus, a consensus has recently emerged that additional treatment strategies are needed. One such strategy is pharmacological neuroprotection, which in the context of glaucoma, refers to the situation in which a drug is deployed to interact with neuronal or glial elements within the retina/optic nerve head and thereby facilitate the survival of RGCs. The advent of animal models of chronic glaucoma has enhanced our understanding of many of the pathological processes occurring in glaucoma and, in doing so, described logical targets for pharmacological intervention. Such targets, which have been manipulated with varying degrees of success in relevant animal paradigms include glutamate receptors, autoimmune elements, neurotrophin deprivation, nitric oxide synthesis, oxidative stress products, sodium and calcium channels, heat shock proteins and apoptotic pathways. With exciting data now emerging from many research laboratories, it is obvious that pharmacological neuroprotection for glaucoma without doubt represents an exciting development in the search for a treatment modality for this debilitating disease.

Indexed as

AnimalsGlaucomaHumansModels, BiologicalNeuroprotective AgentsNeuroprotective Agents

Identifiers

PMID17385943
OpenAlexW2015478081

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.