Evidence map›Paper›PMID 25290063›Full record

ArticleASN neuro2014

A new model of cuprizone-mediated demyelination/remyelination.

Hilary H Sachs, Kathryn K Bercury, Daniela C Popescu, S Priya Narayanan, Wendy B Macklin

Open access · goldAbstract read
In one paragraph

Article in ASN neuro, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Pooled it
  2. Article
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15 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Hilary H SachsDepartment of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, USA.
Kathryn K BercuryDepartment of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, USA.
Daniela C PopescuDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
S Priya NarayananDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Wendy B MacklinDepartment of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, USA Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA wendy.macklin@ucdenver.edu.
Cleveland Clinic Lerner College of Medicine · USUniversity of Colorado Denver · US

Funding

Colorado Clinical and Translational Sciences InstituteUL1TR001082 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2013 to 2017
$48.0M
The role of mTOR signaling in oligodendrocyte differentiation and CNS myelinationR37NS082203 · NINDS · UNIVERSITY OF COLORADO DENVER · PI MACKLIN, WENDY B, WOOD, TERESA L · 2017 to 2023
$6.0M
The role of mTOR signaling in oligodendrocyte differentiation and CNS myelinationR01NS082203 · NINDS · UNIVERSITY OF COLORADO DENVER · PI MACKLIN, WENDY B, WOOD, TERESA L · 2012 to 2016
$3.3M
Signaling pathways controlling myelinationR01NS056417 · NINDS · UNIVERSITY OF COLORADO DENVER · PI MACKLIN, WENDY B · 2007 to 2011
$1.6M
NCATS NIH HHS UL1 TR001082NINDS NIH HHS NS056417NINDS NIH HHS NS082203NINDS NIH HHS R01 NS056417NINDS NIH HHS R01 NS082203
6 · The paper itself

Abstract

In the central nervous system, demyelinating diseases, such as multiple sclerosis, result in devastating long-term neurologic damage, in part because of the lack of effective remyelination in the adult human brain. One model used to understand the mechanisms regulating remyelination is cuprizone-induced demyelination, which allows investigation of remyelination mechanisms in adult animals following toxin-induced demyelination. Unfortunately, the degree of demyelination in the cuprizone model can vary, which complicates understanding the process of remyelination. Previous work in our laboratory demonstrated that the Akt/mTOR pathway regulates active myelination. When given to young postnatal mice, the mTOR inhibitor, rapamycin, inhibits active myelination. In the current study, the cuprizone model was modified by the addition of rapamycin during cuprizone exposure. When administered together, cuprizone and rapamycin produced more complete demyelination and provided a longer time frame over which to investigate remyelination than treatment with cuprizone alone. The consistency in demyelination will allow a better understanding of the mechanisms initiating remyelination. Furthermore, the slower rate of remyelination provides a longer window of time in which to investigate the diverse contributing factors that regulate remyelination. This new model of cuprizone-induced demyelination could potentially aid in identification of new therapeutic targets to enhance remyelination in demyelinating diseases.

Indexed as

Analysis of VarianceAnimalsBasic Helix-Loop-Helix ProteinsBody WeightBrainCuprizoneDemyelinating DiseasesDisease Models, AnimalImmunosuppressive AgentsKi-67 AntigenMaleMiceMice, Inbred C57BLMonoamine Oxidase InhibitorsMyelin-Oligodendrocyte GlycoproteinMyelin SheathBasic Helix-Loop-Helix ProteinsCuprizoneImmunosuppressive AgentsKi-67 AntigenMonoamine Oxidase InhibitorsMyelin-Oligodendrocyte GlycoproteinNerve Tissue ProteinsOlig2 protein, mouseOligodendrocyte Transcription Factor 2Receptor, Platelet-Derived Growth Factor alphaSirolimusAktcuprizonedemyelinationmTORoligodendrocyterapamycin

Identifiers

PMID25290063
PMCPMC4187018
OpenAlexW2170971266

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.