Evidence map›Paper›PMID 27333888›Full record

ReviewCellular and molecular life sciences : CMLS2016

One protein, multiple pathologies: multifaceted involvement of amyloid β in neurodegenerative disorders of the brain and retina.

Vivek Gupta, Veer B Gupta, Nitin Chitranshi, Sumudu Gangoda, Roshana Vander Wall, Mojdeh Abbasi, Mojtaba Golzan, Yogita Dheer, Tejal Shah, Alberto Avolio and 3 more

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
5.6field-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.

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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Damage-Associated Molecular Patterns (DAMPs) in Retinal Disorders.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Transneuronal Degeneration in the Brain During Glaucoma.Frontiers in aging neuroscience · 2021
    Review
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

13 authors at 3 institutions in 1 country.

Vivek GuptaFaculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Veer B GuptaSchool of Medical Sciences, Edith Cowan University, Perth, Australia. v.gupta@ecu.edu.au.
Nitin ChitranshiFaculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Sumudu GangodaFaculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Roshana Vander WallFaculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Mojdeh AbbasiFaculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Mojtaba GolzanFaculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Yogita DheerFaculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Tejal ShahSchool of Medical Sciences, Edith Cowan University, Perth, Australia.
Alberto AvolioFaculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Roger ChungFaculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Ralph MartinsSchool of Medical Sciences, Edith Cowan University, Perth, Australia.
Stuart GrahamFaculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Macquarie University · AUEdith Cowan University · AUUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulation of amyloid β (Aβ) and its aggregates in the ageing central nervous system is regarded synonymous to Alzheimer's disease (AD) pathology. Despite unquestionable advances in mechanistic and diagnostic aspects of the disease understanding, the primary cause of Aβ accumulation as well as its in vivo roles remains elusive; nonetheless, the majority of the efforts to address pathological mechanisms for therapeutic development are focused towards moderating Aβ accumulation in the brain. More recently, Aβ deposition has been identified in the eye and is linked with distinct age-related diseases including age-related macular degeneration, glaucoma as well as AD. Awareness of the Aβ accumulation in these markedly different degenerative disorders has led to an increasing body of work exploring overlapping mechanisms, a prospective biomarker role for Aβ and the potential to use retina as a model for brain related neurodegenerative disorders. Here, we present an integrated view of current understanding of the retinal Aβ deposition discussing the accumulation mechanisms, anticipated impacts and outlining ameliorative approaches that can be extrapolated to the retina for potential therapeutic benefits. Further longitudinal investigations in humans and animal models will determine retinal Aβ association as a potential pathognomonic, diagnostic or prognostic biomarker.

Indexed as

Amyloid beta-PeptidesAnimalsBrainHumansInflammationNeurodegenerative DiseasesProtein AggregatesRetinaAmyloid beta-PeptidesProtein AggregatesElectroretinogramInflammationMetal ionsMitochondrial impairmentNeurotrophic factorsOptical coherence tomographyOxidative stressProtein aggregationVascular dysfunction

Identifiers

PMID27333888
PMCPMC11108534
OpenAlexW2465561348

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.