Evidence map›Paper›PMID 35534594›Full record

ArticleScientific reports2022

Characterization of retinal function and structure in the MPTP murine model of Parkinson's disease.

Katie K N Tran, Vickie H Y Wong, Jeremiah K H Lim, Ali Shahandeh, Anh Hoang, David I Finkelstein, Bang V Bui, Christine T O Nguyen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-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

12 citing papers in PubMed, 19 citations in OpenAlex.

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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 1 institution in 1 country.

Katie K N TranOcular Biomarkers Laboratory, Department of Optometry and Vision Sciences, University of Melbourne, Parkville, VIC, 3010, Australia.
Vickie H Y WongOcular Biomarkers Laboratory, Department of Optometry and Vision Sciences, University of Melbourne, Parkville, VIC, 3010, Australia.ORCID 0000-0001-9356-7556
Jeremiah K H LimOcular Biomarkers Laboratory, Department of Optometry and Vision Sciences, University of Melbourne, Parkville, VIC, 3010, Australia.
Ali ShahandehOcular Biomarkers Laboratory, Department of Optometry and Vision Sciences, University of Melbourne, Parkville, VIC, 3010, Australia.
Anh HoangOcular Biomarkers Laboratory, Department of Optometry and Vision Sciences, University of Melbourne, Parkville, VIC, 3010, Australia.
David I FinkelsteinParkinson's Disease Laboratory, The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, 3010, Australia.
Bang V BuiOcular Biomarkers Laboratory, Department of Optometry and Vision Sciences, University of Melbourne, Parkville, VIC, 3010, Australia.ORCID 0000-0001-7298-1352
Christine T O NguyenOcular Biomarkers Laboratory, Department of Optometry and Vision Sciences, University of Melbourne, Parkville, VIC, 3010, Australia. christine.nguyen@unimelb.edu.au.ORCID 0000-0002-3298-3086
The University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to well characterized motor symptoms, visual disturbances are increasingly recognized as an early manifestation in Parkinson's disease (PD). A better understanding of the mechanisms underlying these changes would facilitate the development of vision tests which can be used as preclinical biomarkers to support the development of novel therapeutics for PD. This study aims to characterize the retinal phenotype of a mouse model of dopaminergic dysfunction and to examine whether these changes are reversible with levodopa treatment. We use a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD to characterize the neurotoxic effects of MPTP on in vivo retinal function (electroretinography, ERG), retinal structure (optical coherence tomography, OCT) and retinal dopaminergic cell number (tyrosine hydroxylase immunohistochemistry, IHC) at two time points (21 and 45 days) post MPTP model induction. We also investigate the effect of levodopa (L-DOPA) as a proof-of-principle chronic intervention against MPTP-induced changes in the retina. We show that MPTP decreases dopaminergic amacrine cell number (9%, p < 0.05) and that a component of the ERG that involves these cells, in particular oscillatory potential (OP) peak timing, was significantly delayed at Day 45 (7-13%, p < 0.01). This functional deficit was paralleled by outer plexiform layer (OPL) thinning (p < 0.05). L-DOPA treatment ameliorated oscillatory potential deficits (7-13%, p < 0.001) in MPTP animals. Our data suggest that the MPTP toxin slows the timing of inner retinal feedback circuits related to retinal dopaminergic pathways which mirrors findings from humans with PD. It also indicates that the MPTP model causes structural thinning of the outer retinal layer on OCT imaging that is not ameliorated with L-DOPA treatment. Together, these non-invasive measures serve as effective biomarkers for PD diagnosis as well as for quantifying the effect of therapy.

Indexed as

MPTP PoisoningParkinson Disease1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAnimalsDisease Models, AnimalDopamineDopaminergic NeuronsLevodopaMiceMice, Inbred C57BLRetinaTyrosine 3-Monooxygenase1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineDopamineLevodopaTyrosine 3-Monooxygenase

Identifiers

PMID35534594
PMCPMC9085791
OpenAlexW4229372171

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.