Evidence map›Paper›PMID 24335072›Full record

ReviewInvestigative ophthalmology & visual science2013

Dry age-related macular degeneration: mechanisms, therapeutic targets, and imaging.

Catherine Bowes Rickman, Sina Farsiu, Cynthia A Toth, Mikael Klingeborn

Open access · bronzeAbstract readReview
In one paragraph

Review in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 2 pooled it
15.5field-weighted citation impact, top 1% 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

156 citing papers in PubMed, 2 syntheses or guidelines pooled it, 276 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Freeze-Dried Extracts ofPreventive nutrition and food science · 2026
    Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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  19. Choroidal Control Technology: New Horizons in Maculopathy and Presbyopia.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025
    Article
  20. Article

96 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 1 institution in 1 country.

Catherine Bowes RickmanDepartment of Ophthalmology, Duke University Medical Center, Durham, North Carolina.
Sina Farsiu
Cynthia A Toth
Mikael Klingeborn
Duke Medical Center · US

Funding

VISION RESEARCHP30EY005722 · NEI · DUKE UNIVERSITY · PI Vadim Y Arshavsky · 1985 to 2026
$19.3M
The APOE TR Mouse: A Model for Elucidating Pathogenic Mechanisms of AMDR01EY019038 · NEI · DUKE UNIVERSITY · PI BOWES RICKMAN, CATHERINE · 2009 to 2014
$2.3M
NEI NIH HHS EY019038NEI NIH HHS P30 EY005722NEI NIH HHS R01 EY019038
6 · The paper itself

Abstract

Age-related macular degeneration is the leading cause of irreversible visual dysfunction in individuals over 65 in Western Society. Patients with AMD are classified as having early stage disease (early AMD), in which visual function is affected, or late AMD (generally characterized as either "wet" neovascular AMD, "dry" atrophic AMD or both), in which central vision is severely compromised or lost. Until recently, there have been no therapies available to treat the disorder(s). Now, the most common wet form of late-stage AMD, choroidal neovascularization, generally responds to treatment with anti-vascular endothelial growth factor therapies. Nevertheless, there are no current therapies to restore lost vision in eyes with advanced atrophic AMD. Oral supplementation with the Age-Related Eye Disease Study (AREDS) or AREDS2 formulation (antioxidant vitamins C and E, lutein, zeaxanthin, and zinc) has been shown to reduce the risk of progression to advanced AMD, although the impact was in neovascular rather than atrophic AMD. Recent findings, however, have demonstrated several features of early AMD that are likely to be druggable targets for treatment. Studies have established that much of the genetic risk for AMD is associated with complement genes. Consequently, several complement-based therapeutic treatment approaches are being pursued. Potential treatment strategies against AMD deposit formation and protein and/or lipid deposition will be discussed, including anti-amyloid therapies. In addition, the role of autophagy in AMD and prevention of oxidative stress through modulation of the antioxidant system will be explored. Finally, the success of these new therapies in clinical trials and beyond relies on early detection, disease typing, and predicting disease progression, areas that are currently being rapidly transformed by improving imaging modalities and functional assays.

Indexed as

Diagnostic Techniques, OphthalmologicalDisease ManagementDry Eye SyndromesMacular DegenerationOxidative StressAngiogenesis InhibitorsAntioxidantsDisease ProgressionHumansAngiogenesis InhibitorsAntioxidantsautophagycomplementdrusenfunctional imagingtherapeutic targets

Identifiers

PMID24335072
PMCPMC3864379
OpenAlexW2117917811

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.