Evidence map›Paper›PMID 33351190›Full record

ArticleThe EMBO journal2021

Netrin-1 and its receptor DCC modulate survival and death of dopamine neurons and Parkinson's disease features.

Mélissa Jasmin, Eun Hee Ahn, Merja H Voutilainen, Joanna Fombonne, Catherine Guix, Tuulikki Viljakainen, Seong Su Kang, Li-Ying Yu, Mart Saarma, Patrick Mehlen and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 73 citations in OpenAlex.

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  13. Implications of draxin in neurological disorders.Frontiers in cell and developmental biology · 2025
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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

11 authors at 3 institutions in 3 countries.

Mélissa JasminApoptosis, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Recherche en Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Centre Léon Bérard, Université de Lyon, Université de Lyon1, Lyon, France.
Eun Hee AhnDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.ORCID 0000-0002-1833-6720
Merja H VoutilainenInstitute of Biotechnology, HiLIFE, University of Helsinki, Helsinki, Finland.
Joanna FombonneApoptosis, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Recherche en Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Centre Léon Bérard, Université de Lyon, Université de Lyon1, Lyon, France.
Catherine GuixApoptosis, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Recherche en Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Centre Léon Bérard, Université de Lyon, Université de Lyon1, Lyon, France.
Tuulikki ViljakainenInstitute of Biotechnology, HiLIFE, University of Helsinki, Helsinki, Finland.
Seong Su KangDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Li-Ying YuInstitute of Biotechnology, HiLIFE, University of Helsinki, Helsinki, Finland.
Mart SaarmaInstitute of Biotechnology, HiLIFE, University of Helsinki, Helsinki, Finland.
Patrick MehlenApoptosis, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Recherche en Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Centre Léon Bérard, Université de Lyon, Université de Lyon1, Lyon, France.ORCID 0000-0003-1743-5417
Keqiang YeDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.ORCID 0000-0002-7657-8154
Université Claude Bernard Lyon 1 · FRUniversity of Helsinki · FIEmory University · US

Funding

Molecular Regulation of AEP during AgeingRF1AG051538 · NIA · EMORY UNIVERSITY · PI YE, KEQIANG · 2016 to 2016
$3.4M
NIA NIH HHS RF1 AG051538
6 · The paper itself

Abstract

The netrin-1/DCC ligand/receptor pair has key roles in central nervous system (CNS) development, mediating axonal, and neuronal navigation. Although expression of netrin-1 and DCC is maintained in the adult brain, little is known about their role in mature neurons. Notably, netrin-1 is highly expressed in the adult substantia nigra, leading us to investigate a role of the netrin-1/DCC pair in adult nigral neuron fate. Here, we show that silencing netrin-1 in the adult substantia nigra of mice induces DCC cleavage and a significant loss of dopamine neurons, resulting in motor deficits. Because loss of adult dopamine neurons and motor impairments are features of Parkinson's disease (PD), we studied the potential impact of netrin-1 in different animal models of PD. We demonstrate that both overexpression of netrin-1 and brain administration of recombinant netrin-1 are neuroprotective and neurorestorative in mouse and rat models of PD. Of interest, we observed that netrin-1 levels are significantly reduced in PD patient brain samples. These results highlight the key role of netrin-1 in adult dopamine neuron fate, and the therapeutic potential of targeting netrin-1 signaling in PD.

Indexed as

AnimalsCell DeathDCC ReceptorDisease Models, AnimalDopaminergic NeuronsDown-RegulationFemaleGene SilencingHumansMaleMiceNetrin-1Parkinson DiseaseRatsSignal TransductionSubstantia NigraDCC protein, humanDCC ReceptorNetrin-1NTN1 protein, humannetrin-1/ DCCneurorestorationParkinson’s disease

Identifiers

PMID33351190
PMCPMC7849168
OpenAlexW3116523795

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.