Evidence map›Paper›PMID 26339673›Full record

ArticleAnnals of clinical and translational neurology2015

Curcumin therapy in a Plp1 transgenic mouse model of Pelizaeus-Merzbacher disease.

Dirk B Epplen, Thomas Prukop, Tobias Nientiedt, Philipp Albrecht, Friederike A Arlt, Ruth M Stassart, Celia M Kassmann, Axel Methner, Klaus-Armin Nave, Hauke B Werner and 1 more

Open access · goldAbstract read
In one paragraph

Article in Annals of clinical and translational neurology, 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
0.8field-weighted citation impact, top 37% 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, 20 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

11 authors at 4 institutions in 1 country.

Dirk B EpplenDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine Göttingen, Germany.
Thomas PrukopDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine Göttingen, Germany ; Institute of Clinical Pharmacology, University Medical Center Göttingen (UMG) Göttingen, Germany.
Tobias NientiedtDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine Göttingen, Germany.
Philipp AlbrechtDepartment of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Germany.
Friederike A ArltDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine Göttingen, Germany.
Ruth M StassartDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine Göttingen, Germany ; Institute of Neuropathology, University Medical Center Göttingen (UMG) Göttingen, Germany.
Celia M KassmannDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine Göttingen, Germany.
Axel MethnerFocus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn2), Department of Neurology, Johannes Gutenberg University Medical Center Mainz Mainz, Germany.
Klaus-Armin NaveDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine Göttingen, Germany.
Hauke B WernerDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine Göttingen, Germany.
Michael W SeredaDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine Göttingen, Germany ; Department of Clinical Neurophysiology, University Medical Center Göttingen (UMG) Göttingen, Germany.
Max Planck Institute of Experimental Medicine · DEUniversitätsmedizin Göttingen · DEHeinrich Heine University Düsseldorf · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePelizaeus-Merzbacher disease (PMD) is a progressive and lethal leukodystrophy caused by mutations affecting the proteolipid protein (PLP1) gene. The most common cause of PMD is a duplication of PLP1 and at present there is no curative therapy available.

methodsBy using transgenic mice carrying additional copies of Plp1, we investigated whether curcumin diet ameliorates PMD symptoms. The diet of Plp1 transgenic mice was supplemented with curcumin for 10 consecutive weeks followed by phenotypical, histological and immunohistochemical analyses of the central nervous system. Plp1 transgenic and wild-type mice fed with normal chow served as controls.

resultsCurcumin improved the motor phenotype performance of Plp1 transgenic mice by 50% toward wild-type level and preserved myelinated axons by 35% when compared to Plp1 transgenic controls. Furthermore, curcumin reduced astrocytosis, microgliosis and lymphocyte infiltration in Plp1 transgenic mice. Curcumin diet did not affect the pathologically increased Plp1 mRNA abundance. However, high glutathione levels indicating an oxidative misbalance in the white matter of Plp1 transgenic mice were restored by curcumin treatment.

interpretationCurcumin may potentially serve as an antioxidant therapy of PMD caused by PLP1 gene duplication.

Identifiers

PMID26339673
PMCPMC4554440
OpenAlexW1562818493

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.