Evidence map›Paper›PMID 23933169›Full record

ReviewProgress in retinal and eye research2013

Aging is not a disease: distinguishing age-related macular degeneration from aging.

Daniel Ardeljan, Chi-Chao Chan

Open access · greenAbstract readReview
In one paragraph

Review in Progress in retinal and eye research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed, 1 pooled it
18.3field-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

141 citing papers in PubMed, 1 synthesis or guideline pooled it, 239 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Calpain-specific breakdown fragment in human drusen.Histology and histopathology · 2024
    Article
  18. Article
  19. Article
  20. Article

81 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 1 institution in 1 country.

Daniel ArdeljanImmunopathology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA; Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address: dardelj1@jhu.edu.
Chi-Chao Chan
National Institutes of Health · US

Funding

Histopathology CoreZICEY000461 · NEI · NATIONAL EYE INSTITUTE · PI SCHNEEWEIS, DAVID · 2009 to 2022
$7.7M
Molecular And Immunopathology Of Experimental And Clinical Ocular DiseasesZIAEY000222 · NEI · NATIONAL EYE INSTITUTE · PI CHAN, CHI-CHAO · 2009 to 2015
$7.2M
Age-Related Macular Degeneration: Genetic Variations and Animal ModelZIAEY000418 · NEI · NATIONAL EYE INSTITUTE · PI CHAN, CHI-CHAO · 2009 to 2015
$6.0M
Intramural NIH HHS ZIA EY000418
6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is a disease of the outer retina, characterized most significantly by atrophy of photoreceptors and retinal pigment epithelium accompanied with or without choroidal neovascularization. Development of AMD has been recognized as contingent on environmental and genetic risk factors, the strongest being advanced age. In this review, we highlight pathogenic changes that destabilize ocular homeostasis and promote AMD development. With normal aging, photoreceptors are steadily lost, Bruch's membrane thickens, the choroid thins, and hard drusen may form in the periphery. In AMD, many of these changes are exacerbated in addition to the development of disease-specific factors such as soft macular drusen. Para-inflammation, which can be thought of as an intermediate between basal and robust levels of inflammation, develops within the retina in an attempt to maintain ocular homeostasis, reflected by increased expression of the anti-inflammatory cytokine IL-10 coupled with shifts in macrophage plasticity from the pro-inflammatory M1 to the anti-inflammatory M2 polarization. In AMD, imbalances in the M1 and M2 populations together with activation of retinal microglia are observed and potentially contribute to tissue degeneration. Nonetheless, the retina persists in a state of chronic inflammation and increased expression of certain cytokines and inflammasomes is observed. Since not everyone develops AMD, the vital question to ask is how the body establishes a balance between normal age-related changes and the pathological phenotypes in AMD.

Indexed as

Macular DegenerationAgingBruch MembraneEye Diseases, HereditaryEye ProteinsHumansLipid MetabolismOxidative StressRetinal DrusenEye ProteinsAge-related macular degenerationAgingHomeostasisOxidative stressPara-inflammationRetina

Identifiers

PMID23933169
PMCPMC3830684
OpenAlexW2068001921

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.