Evidence map›Paper›PMID 22396019›Full record

ArticleMolecular medicine (Cambridge, Mass.)2012

Erythropoietin attenuates neurological and histological consequences of toxic demyelination in mice.

Nora Hagemeyer, Susann Boretius, Christoph Ott, Axel Von Streitberg, Henrike Welpinghus, Swetlana Sperling, Jens Frahm, Mikael Simons, Pietro Ghezzi, Hannelore Ehrenreich

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-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

23 citing papers in PubMed, 46 citations in OpenAlex.

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  17. A double-blind, placebo-controlled trial of adding erythropoietin to intravenous methylprednisolone for the treatment of unilateral acute optic neuritis of unknown or demyelinative origin.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2015
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  19. Immunosuppressive effects of erythropoietin on human alloreactive T cells.Journal of the American Society of Nephrology : JASN · 2014
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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

10 authors at 3 institutions in 2 countries.

Nora HagemeyerDivision of Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Susann Boretius
Christoph Ott
Axel Von Streitberg
Henrike Welpinghus
Swetlana Sperling
Jens Frahm
Mikael Simons
Pietro Ghezzi
Hannelore Ehrenreich
Max Planck Institute of Experimental Medicine · DEMax Planck Institute for Biophysical Chemistry · DEBrighton and Sussex Medical School · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Erythropoietin (EPO) reduces symptoms of experimental autoimmune encephalomyelitis in rodents and shows neuroregenerative effects in chronic progressive multiple sclerosis. The mechanisms of action of EPO in these conditions with shared immunological etiology are still unclear. Therefore, we used a model of toxic demyelination allowing exclusion of T cell-mediated inflammation. In a double-blind (for food/injections), placebo-controlled, longitudinal four-arm design, 8-wk-old C57BL/6 mice (n = 26/group) were assigned to cuprizone-containing (0.2%) or regular food (ground chow) for 6 wks. After 3 wks, mice were injected every other day with placebo or EPO (5,000 IU/kg intraperitoneally) until the end of cuprizone feeding. Half of the mice were exposed to behavioral testing, magnetic resonance imaging (MRI) and histology immediately after treatment cessation, whereas the other half were allowed a 3-wk treatment-free recovery. Immediately after termination of cuprizone feeding, all toxin-exposed mice were compromised regarding vestibulomotor function/coordination, with EPO-treated animals performing better than placebo. Likewise, ventricular enlargement after cuprizone, as documented by MRI, was less pronounced upon EPO. After a 3-wk recovery, remarkable spontaneous improvement was observed in all mice with no measurable further benefit in the EPO group ("ceiling effect"). Histological analysis of the corpus callosum revealed attenuation by EPO of the cuprizone-induced increase in microglial numbers and amyloid precursor protein accumulations as a readout of inflammation and axonal degeneration. To conclude, EPO ameliorates neurological symptoms in the cuprizone model of demyelination, possibly by reduction of inflammation-associated axonal degeneration in white matter tracts. These findings underscore the value of future therapeutic strategies for multiple sclerosis based on EPO or EPO variants.

Indexed as

Amyloid beta-Protein PrecursorAnimalsAxonsCerebral VentriclesCorpus CallosumCuprizoneDemyelinating DiseasesErythropoietinInflammationMaleMiceMice, Inbred C57BLMicrogliaNeuroprotective AgentsPostural BalancePsychomotor PerformanceAmyloid beta-Protein PrecursorCuprizoneErythropoietinNeuroprotective Agents

Identifiers

PMID22396019
PMCPMC3388128
OpenAlexW1777347610

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.