Evidence map›Paper›PMID 27955999›Full record

ReviewExperimental eye research2017

Neuroprotection for glaucoma: Requirements for clinical translation.

Leonard A Levin, Megan E Crowe, Harry A Quigley, Lasker/IRRF Initiative on Astrocytes and Glaucomatous Neurodegeneration Participants

Open access · greenAbstract readReview
In one paragraph

Review in Experimental eye research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Protective Effects of Lipoxin AbioRxiv : the preprint server for biology · 2024
    Article
  7. Article
  8. Potential role ofNeural regeneration research · 2023
    Article
  9. Article
  10. Observational
  11. Distinct Role ofPharmaceuticals (Basel, Switzerland) · 2023
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
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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 5 institutions in 2 countries.

Leonard A LevinDepartment of Ophthalmology, McGill University, Montreal, Quebec, Canada; Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Electronic address: lalevin@wisc.edu.
Megan E CroweDepartment of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Harry A QuigleyWilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Lasker/IRRF Initiative on Astrocytes and Glaucomatous Neurodegeneration Participants
Johns Hopkins University · USMadison Group (United States) · USPhiladelphia University · USUniversity of Baltimore · USUniversity of Wisconsin–Madison · US

Funding

Wilmer Core Grant for Vision ResearchP30EY001765 · NEI · JOHNS HOPKINS UNIVERSITY · PI Ji Yi · 1985 to 2026
$22.1M
PATHOGENESIS OF GLAUCOMATOUS OPTIC NERVE DAMAGER01EY002120 · NEI · JOHNS HOPKINS UNIVERSITY · PI QUIGLEY, HARRY ALAN · 1985 to 2025
$12.6M
UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI Donna M Peters · 2005 to 2026
$12.6M
Development of redox-active therapies for ischemic optic neuropathyR21EY025074 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI LEVIN, LEONARD A · 2015 to 2016
$421k
NEI NIH HHS P30 EY001765NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY002120NEI NIH HHS R21 EY025074
6 · The paper itself

Abstract

Within the field of glaucoma research, neuroprotection is defined as slowing the functional loss in glaucoma by a mechanism independent of lowering of intraocular pressure. There is currently a great potential for research surrounding neuroprotection as it relates to glaucoma. Anatomical targets for neuroprotection should focus on upstream rather than downstream factors, and could include any part of the retinal ganglion cell, the glia, especially astrocytes or Muller cells, and vasculature. The great number of anatomical targets is exceeded only by the number of possible biochemical pathways and potential treatments. Successful treatment may be accomplished through the targeting of one or even a combination of multiple pathways. Once a treatment is shown effective in vitro, it should be evaluated in vivo with carefully chosen animal models and studied in sufficient numbers to detect statistically and clinically significant effects. Such a drug should have few systemic side effects and its delivery should be optimized so as to encourage compliance. There are still a multitude of possible screens available to test the efficacy of a neuroprotective drug and a single gold standard is ideal for the accurate assessment and comparison of new drugs. Future studies in neuroprotection should investigate the genetic component of the disease, novel pharmaceutical agents for new or known pathways, modulations of scleral biomechanics, and relation to research of other complex disorders of the central nervous system.

Indexed as

Translational Research, BiomedicalAnimalsAstrocytesAxonsGlaucomaHumansNeuroprotectionNeuroprotective AgentsOptic Nerve DiseasesRetinal Ganglion CellsNeuroprotective AgentsAstrocytesAxonsGlaucomaNeuroprotectionRetinal ganglion cells

Identifiers

PMID27955999
PMCPMC5413382
OpenAlexW2560420095

What OpenQuestion holds

Textmetadata
LicenceTDM
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.