Evidence map›Paper›PMID 26099628›Full record

ArticleMolecular neurodegeneration2015

Nigral overexpression of alpha-synuclein in the absence of parkin enhances alpha-synuclein phosphorylation but does not modulate dopaminergic neurodegeneration.

Anne-Sophie Van Rompuy, Marusela Oliveras-Salvá, Anke Van der Perren, Olga Corti, Chris Van den Haute, Veerle Baekelandt

Open access · goldAbstract readComparative Study
In one paragraph

Article in Molecular neurodegeneration, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  3. Analysis of α-syn andFrontiers in cellular neuroscience · 2023
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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

6 authors at 2 institutions in 2 countries.

Anne-Sophie Van RompuyLaboratory for Neurobiology and Gene Therapy, Department of Neurosciences, KU Leuven, Flanders, Belgium. annexsophie.vanrompuy@uzleuven.be.
Marusela Oliveras-SalváLaboratory for Neurobiology and Gene Therapy, Department of Neurosciences, KU Leuven, Flanders, Belgium.
Anke Van der PerrenLaboratory for Neurobiology and Gene Therapy, Department of Neurosciences, KU Leuven, Flanders, Belgium. Anke.VanderPerren@med.kuleuven.be.
Olga CortiInserm, U 975, CRICM, Hôpital de la Pitié-Salpêtrière, F-75013, Paris, France. olga.corti@upmc.fr.
Chris Van den HauteLaboratory for Neurobiology and Gene Therapy, Department of Neurosciences, KU Leuven, Flanders, Belgium. Chris.VanDenHaute@med.kuleuven.be.
Veerle BaekelandtLaboratory for Neurobiology and Gene Therapy, Department of Neurosciences, KU Leuven, Flanders, Belgium. Veerle.Baekelandt@med.kuleuven.be.
KU Leuven · BEInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlpha-synuclein is a key protein in the pathogenesis of Parkinson's disease. Mutations in the parkin gene are the most common cause of early-onset autosomal recessive Parkinson's disease, probably through a loss-of-function mechanism. However, the molecular mechanism by which loss of parkin function leads to the development of the disease and the role of alpha-synuclein in parkin-associated Parkinson's disease is still not elucidated. Conflicting results were reported about the effect of the absence of parkin on alpha-synuclein-mediated neurotoxicity using a transgenic approach. In this study, we investigated the effect of loss of parkin on alpha-synuclein neuropathology and toxicity in adult rodent brain using viral vectors. Therefore, we overexpressed human wild type alpha-synuclein in the substantia nigra of parkin knockout and wild type mice using two different doses of recombinant adeno-associated viral vectors.

resultsNo difference was observed in nigral dopaminergic cell loss between the parkin knockout mice and wild type mice up to 16 weeks after viral vector injection. However, the level of alpha-synuclein phosphorylated at serine residue 129 in the substantia nigra was significantly increased in the parkin knockout mice compared to the wild type mice while the total expression level of alpha-synuclein was similar in both groups. The increased alpha-synuclein phosphorylation was confirmed in a parkin knockdown cell line.

conclusionsThese findings support a functional relationship between parkin and alpha-synuclein phosphorylation in rodent brain.

Indexed as

Protein Processing, Post-Translationalalpha-SynucleinAnimalsCell CountCell Line, TumorDependovirusDopaminergic NeuronsFemaleGenes, ReporterGenetic VectorsHumansLentivirusMaleMiceMice, Inbred C57BLMice, Knockoutalpha-SynucleinMicroRNAsparkin proteinPhosphoserineUbiquitin-Protein Ligases

Identifiers

PMID26099628
PMCPMC4477319
OpenAlexW1845531777

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.