Evidence map›Paper›PMID 27551275›Full record

ReviewFrontiers in neurology2016

Amyloidosis in Retinal Neurodegenerative Diseases.

Ambra Masuzzo, Virginie Dinet, Chelsea Cavanagh, Frederic Mascarelli, Slavica Krantic

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  15. Review
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  17. Article
  18. Retinal Degeneration and Alzheimer's Disease: An Evolving Link.International journal of molecular sciences · 2020
    Review
  19. Review
  20. Article
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

5 authors at 2 institutions in 2 countries.

Ambra MasuzzoCentre de Recherche des Cordeliers, Institut national de la santé et de la recherche médicale (INSERM), Université Paris Descartes, Sorbonne Paris Cité, UMR_S 1138, Université Pierre et Marie Curie Université Paris 06, Sorbonne Universités , Paris , France.
Virginie DinetCentre de Recherche des Cordeliers, Institut national de la santé et de la recherche médicale (INSERM), Université Paris Descartes, Sorbonne Paris Cité, UMR_S 1138, Université Pierre et Marie Curie Université Paris 06, Sorbonne Universités , Paris , France.
Chelsea CavanaghDepartment of Neuroscience, Douglas Hospital Research Center , Montreal, QC , Canada.
Frederic MascarelliCentre de Recherche des Cordeliers, Institut national de la santé et de la recherche médicale (INSERM), Université Paris Descartes, Sorbonne Paris Cité, UMR_S 1138, Université Pierre et Marie Curie Université Paris 06, Sorbonne Universités , Paris , France.
Slavica KranticCentre de Recherche des Cordeliers, Institut national de la santé et de la recherche médicale (INSERM), Université Paris Descartes, Sorbonne Paris Cité, UMR_S 1138, Université Pierre et Marie Curie Université Paris 06, Sorbonne Universités , Paris , France.
Centre de Recherche des Cordeliers · FRDouglas Mental Health University Institute · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a part of the central nervous system, the retina may reflect both physiological processes and abnormalities related to pathologies that affect the brain. Amyloidosis due to the accumulation of amyloid-beta (Aβ) was initially regarded as a specific and exclusive characteristic of neurodegenerative alterations seen in the brain of Alzheimer's disease (AD) patients. More recently, it was discovered that amyloidosis-related alterations, similar to those seen in the brain of Alzheimer's patients, also occur in the retina. Remarkably, these alterations were identified not only in primary retinal pathologies, such as age-related macular degeneration (AMD) and glaucoma, but also in the retinas of Alzheimer's patients. In this review, we first briefly discuss the biogenesis of Aβ, a peptide involved in amyloidosis. We then discuss some pathological aspects (synaptic dysfunction, mitochondrial failure, glial activation, and vascular abnormalities) related to the neurotoxic effects of Aβ. We finally highlight common features shared by AD, AMD, and glaucoma in the context of Aβ amyloidosis and further discuss why the retina, due to the transparency of the eye, can be considered as a "window" to the brain.

Indexed as

age-related macular degenerationAlzheimer’s diseaseglaucomamicoangiopathyneurodegenerationneuroinflammationsynaptic and mitochondrial dysfunction

Identifiers

PMID27551275
PMCPMC4976396
OpenAlexW2515864126

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.