Evidence map›Paper›PMID 30796158›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

Translocator Protein Ligand Protects against Neurodegeneration in the MPTP Mouse Model of Parkinsonism.

Jing Gong, Éva M Szego, Andrei Leonov, Eva Benito, Stefan Becker, Andre Fischer, Markus Zweckstetter, Tiago Outeiro, Anja Schneider

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 68 citations in OpenAlex.

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  17. Histamine Causes Pyroptosis of Liver by Regulating Gut-Liver Axis in Mice.International journal of molecular sciences · 2022
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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

9 authors at 4 institutions in 2 countries.

Jing GongGerman Center for Neurodegenerative Diseases, 53127 Bonn, Germany.ORCID 0000-0002-2575-3899
Éva M SzegoDepartment of Experimental Neurodegeneration, Center for Biostructural Imaging of Neurodegeneration, University Medical Center Göttingen, University of Göttingen, 37075 Göttingen, Germany.
Andrei LeonovMax-Planck-Institute for Biophysical Chemistry, 37077 Göttingen, Germany.
Eva BenitoGerman Center for Neurodegenerative Diseases, 37075 Göttingen, Germany.ORCID 0000-0003-0094-0257
Stefan BeckerMax-Planck-Institute for Biophysical Chemistry, 37077 Göttingen, Germany.
Andre FischerGerman Center for Neurodegenerative Diseases, 37075 Göttingen, Germany.
Markus ZweckstetterCluster of Excellence, Nanoscale Microscopy and Molecular Physiology of the Brain, 30703 Göttingen, Germany.ORCID 0000-0002-2536-6581
Tiago OuteiroDepartment of Experimental Neurodegeneration, Center for Biostructural Imaging of Neurodegeneration, University Medical Center Göttingen, University of Göttingen, 37075 Göttingen, Germany.ORCID 0000-0003-1679-1727
Anja SchneiderGerman Center for Neurodegenerative Diseases, 53127 Bonn, Germany, anja.schneider@dzne.de.
German Center for Neurodegenerative Diseases · DEMax Planck Institute for Biophysical Chemistry · DEUniversitätsmedizin Göttingen · DEUniversity Hospital Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease is the second most common neurodegenerative disease, after Alzheimer's disease. Parkinson's disease is a movement disorder with characteristic motor features that arise due to the loss of dopaminergic neurons from the substantia nigra. Although symptomatic treatment by the dopamine precursor levodopa and dopamine agonists can improve motor symptoms, no disease-modifying therapy exists yet. Here, we show that Emapunil (AC-5216, XBD-173), a synthetic ligand of the translocator protein 18, ameliorates degeneration of dopaminergic neurons, preserves striatal dopamine metabolism, and prevents motor dysfunction in female mice treated with the MPTP, as a model of parkinsonism. We found that Emapunil modulates the inositol requiring kinase 1α (IRE α)/X-box binding protein 1 (XBP1) unfolded protein response pathway and induces a shift from pro-inflammatory toward anti-inflammatory microglia activation. Previously, Emapunil was shown to cross the blood-brain barrier and to be safe and well tolerated in a Phase II clinical trial. Therefore, our data suggest that Emapunil may be a promising approach in the treatment of Parkinson's disease.

Indexed as

AnimalsCorpus StriatumFemaleHumansLigandsMiceMice, Inbred C57BLNeurodegenerative DiseasesNeuroprotective AgentsParkinsonian DisordersPurinesReceptors, GABABzrp protein, mouseLigandsN-benzyl-N-ethyl-2-(7,8-dihydro-7-methyl-8-oxo-2-phenyl-9H-purin-9-yl)acetamideNeuroprotective AgentsPurinesReceptors, GABAmicrogliaMPTPneurodegenerationParkinson's diseaseTSPO

Identifiers

PMID30796158
PMCPMC6510339
OpenAlexW2917383181

What OpenQuestion holds

Textmetadata
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.