Evidence map›Paper›PMID 28740252›Full record

ArticleScientific reports2017

Decelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model.

J Teister, F Anders, S Beck, S Funke, H von Pein, V Prokosch, N Pfeiffer, F Grus

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

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  13. Hydrogen Sulfide andJournal of ophthalmology · 2020
    Article
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  16. [Autoimmunity and glaucoma].Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 2019
    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

8 authors at 2 institutions in 1 country.

J TeisterExperimental Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University, 55131, Mainz, Germany.
F AndersExperimental Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University, 55131, Mainz, Germany.
S BeckExperimental Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University, 55131, Mainz, Germany.
S FunkeExperimental Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University, 55131, Mainz, Germany.
H von PeinInstitute of Neuropathology, University Medical Center of the Johannes Gutenberg University, 55131, Mainz, Germany.
V ProkoschExperimental Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University, 55131, Mainz, Germany.
N PfeifferExperimental Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University, 55131, Mainz, Germany.
F GrusExperimental Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University, 55131, Mainz, Germany. grus@eye-research.org.
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although elevated intraocular pressure (IOP) remains the major risk factor in glaucoma, neurodegenerative processes continue despite effective IOP lowering. Altered α-synuclein antibody (Abs) levels have been reported to play a crucial role. This study aimed at identifying whether α-synuclein Abs are capable to decelerate neuronal decay while providing insights into proteomic changes. Four groups of Sprague Dawley rats received episcleral vein occlusion: (1) CTRL, no intravitreal injection, n = 6, (2) CTRL IgG, intravitreal injection of unspecific IgG, n = 5, (3) Buffer, intravitreal injection of buffer, n = 6, (4), α-synuclein Ab, intravitreal injection of α-synuclein Ab, n = 5. IOP and retinal nerve fiber layer thickness (RNFLT) were monitored and immunohistochemistry, microarray and proteomic analysis were performed. RNFLT was reduced in CTRL, CTRL IgG and Buffer group (all p < 0.01) and α-synuclein Ab group (p = 0.17). Axon and RGC density showed an increased neurodegeneration in CTRL, CTRL IgG and Buffer group (all p < 0.01) and increased neuronal survival in α-synuclein Ab group (p = 0.38 and 0.06, respectively) compared with fellow eyes. Proteomic analysis revealed alterations of cofilin 1 and superoxide dismutase 1 expression. This data indicate that α-synuclein Ab might indirectly modulate the actin cytoskeleton organization and negatively regulate apoptotic processes via cofilin 1 and superoxide dismutase 1.

Indexed as

alpha-SynucleinAnimalsAntibodies, MonoclonalApoptosisDecelerationDisease Models, AnimalFemaleGlaucomaIntraocular PressureIntravitreal InjectionsNerve DegenerationNeuroprotective AgentsProteomicsRatsRats, Sprague-DawleyRetinaalpha-SynucleinAntibodies, MonoclonalNeuroprotective AgentsSnca protein, rat

Identifiers

PMID28740252
PMCPMC5524683
OpenAlexW2738285462

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.