Evidence map›Paper›PMID 31840869›Full record

ArticleMovement disorders : official journal of the Movement Disorder Society2020

Glial cell line-derived neurotrophic factor receptor Rearranged during transfection agonist supports dopamine neurons in Vitro and enhances dopamine release In Vivo.

Arun Kumar Mahato, Jaakko Kopra, Juho-Matti Renko, Tanel Visnapuu, Ilari Korhonen, Nita Pulkkinen, Maxim M Bespalov, Andrii Domanskyi, Eric Ronken, T Petteri Piepponen and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Movement disorders : official journal of the Movement Disorder Society, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Organosulfur Compounds: Potential Therapeutics for Parkinson's Disease.CNS & neurological disorders drug targets · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Biological ActivityBiomacromolecules · 2023
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

15 authors at 4 institutions in 4 countries.

Arun Kumar MahatoLaboratory of Molecular Neuroscience, Institute of Biotechnology, Helsinki Institute of Life Science, Viikinkaari 5D, University of Helsinki, Helsinki, Finland.
Jaakko KopraDivision of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, Viikinkaari 5E, University of Helsinki, Helsinki, Finland.
Juho-Matti RenkoDivision of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, Viikinkaari 5E, University of Helsinki, Helsinki, Finland.
Tanel VisnapuuDivision of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, Viikinkaari 5E, University of Helsinki, Helsinki, Finland.
Ilari KorhonenDivision of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, Viikinkaari 5E, University of Helsinki, Helsinki, Finland.
Nita PulkkinenDivision of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, Viikinkaari 5E, University of Helsinki, Helsinki, Finland.
Maxim M BespalovLaboratory of Molecular Neuroscience, Institute of Biotechnology, Helsinki Institute of Life Science, Viikinkaari 5D, University of Helsinki, Helsinki, Finland.
Andrii DomanskyiLaboratory of Molecular Neuroscience, Institute of Biotechnology, Helsinki Institute of Life Science, Viikinkaari 5D, University of Helsinki, Helsinki, Finland.
Eric RonkenSolvay Pharmaceuticals, Weesp, Netherlands.
T Petteri PiepponenDivision of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, Viikinkaari 5E, University of Helsinki, Helsinki, Finland.
Merja H VoutilainenLaboratory of Molecular Neuroscience, Institute of Biotechnology, Helsinki Institute of Life Science, Viikinkaari 5D, University of Helsinki, Helsinki, Finland.
Raimo K TuominenDivision of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, Viikinkaari 5E, University of Helsinki, Helsinki, Finland.
Mati KarelsonInstitute of Chemistry, Tartu University, Tartu, Estonia.
Yulia A SidorovaLaboratory of Molecular Neuroscience, Institute of Biotechnology, Helsinki Institute of Life Science, Viikinkaari 5D, University of Helsinki, Helsinki, Finland.
Mart SaarmaLaboratory of Molecular Neuroscience, Institute of Biotechnology, Helsinki Institute of Life Science, Viikinkaari 5D, University of Helsinki, Helsinki, Finland.
University of Helsinki · FIInstitute for Molecular Medicine Finland · FISolvay (Belgium) · BEUniversity of Tartu · EE

Funding

Parkinson's UK K-1408
6 · The paper itself

Abstract

backgroundMotor symptoms of Parkinson's disease (PD) are caused by degeneration and progressive loss of nigrostriatal dopamine neurons. Currently, no cure for this disease is available. Existing drugs alleviate PD symptoms but fail to halt neurodegeneration. Glial cell line-derived neurotrophic factor (GDNF) is able to protect and repair dopamine neurons in vitro and in animal models of PD, but the clinical use of GDNF is complicated by its pharmacokinetic properties. The present study aimed to evaluate the neuronal effects of a blood-brain-barrier penetrating small molecule GDNF receptor Rearranged in Transfection agonist, BT13, in the dopamine system.

methodsWe characterized the ability of BT13 to activate RET in immortalized cells, to support the survival of cultured dopamine neurons, to protect cultured dopamine neurons against neurotoxin-induced cell death, to activate intracellular signaling pathways both in vitro and in vivo, and to regulate dopamine release in the mouse striatum as well as BT13's distribution in the brain.

resultsBT13 potently activates RET and downstream signaling cascades such as Extracellular Signal Regulated Kinase and AKT in immortalized cells. It supports the survival of cultured dopamine neurons from wild-type but not from RET-knockout mice. BT13 protects cultured dopamine neurons from 6-Hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium (MPP

conclusionThe GDNF receptor RET agonist BT13 demonstrates the potential for further development of novel disease-modifying treatments against PD. © 2019 International Parkinson and Movement Disorder Society.

Indexed as

AnimalsCorpus StriatumDopamineDopaminergic NeuronsGlial Cell Line-Derived Neurotrophic FactorGlial Cell Line-Derived Neurotrophic Factor ReceptorsMiceOxidopamineParkinson DiseaseParkinson Disease, SecondarySubstantia NigraDopamineGlial Cell Line-Derived Neurotrophic FactorGlial Cell Line-Derived Neurotrophic Factor ReceptorsOxidopamineClustered Regularly Interspaced Short Palindromic Repeats/CRISPR associated protein 9dopamine neuronsglial cell line-derived neurotrophic factor (GDNF)Parkinson's diseasereceptor tyrosine kinase RET agonist

Identifiers

PMID31840869
PMCPMC7496767
OpenAlexW2995037816

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.