Evidence map›Paper›PMID 21187126›Full record

ReviewNeuroscience2011

Neurodegeneration in glaucoma: progression and calcium-dependent intracellular mechanisms.

S D Crish, D J Calkins

Abstract readReview
In one paragraph

Review in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
6.8field-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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Role of store-operated CaFrontiers in aging neuroscience · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Adaptive responses to neurodegenerative stress in glaucoma.Progress in retinal and eye research · 2021
    Review
  16. Review
  17. Energy Metabolism in the Inner Retina in Health and Glaucoma.International journal of molecular sciences · 2021
    Review
  18. Review
  19. Review
  20. Article

23 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

2 authors at 2 institutions in 1 country.

S D CrishDepartment of Pharmaceutical Sciences, Northeastern Ohio Universities Colleges of Medicine and Pharmacy, Rootstown, OH 44272, USA.
D J Calkins
Northeast Ohio Medical University · USVanderbilt University Medical Center · US

Funding

Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kevin L Schey · 1989 to 2026
$19.6M
Transient Receptor Potential Channels and Retinal Ganglion Cell Death in GlaucomaR01EY017427 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CALKINS, DAVID J. · 2008 to 2020
$4.2M
NEI NIH HHS EY017427NEI NIH HHS P30 EY008126NEI NIH HHS P30EY008126NEI NIH HHS R01 EY017427
6 · The paper itself

Abstract

Glaucoma is an age-related optic neuropathy involving sensitivity to ocular pressure. The disease is now seen increasingly as one of the central nervous system, as powerful new approaches highlight an increasing number of similarities with other age-related neurodegenerations such as Alzheimer's and Parkinson's. While the etiologies of these diseases are diverse, they involve many important common elements including compartmentalized programs of degeneration targeting axons, dendrites and finally cell bodies. Most age-related degenerations display early functional deficits that precede actual loss of neuronal substrate. These are linked to several specific neurochemical cascades that can be linked back to dysregulation of Ca(2+)-dependent processes. We are now in the midst of identifying similar cascades in glaucoma. Here we review recent evidence on the pathological progression of neurodegeneration in glaucoma and some of the Ca(2+)-dependent mechanisms that could underlie these changes. These mechanisms present clear implications for efforts to develop interventions targeting neuronal loss directly and make glaucoma an attractive model for both interrogating and informing other neurodegenerative diseases.

Indexed as

CalciumDisease ProgressionGlaucomaHumansIntracellular SpaceNerve DegenerationCalcium

Identifiers

PMID21187126
PMCPMC3040267
OpenAlexW2072918492

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.