Evidence map›Paper›PMID 18835867›Full record

ArticleBrain : a journal of neurology2008

Granulocyte-colony stimulating factor improves outcome in a mouse model of amyotrophic lateral sclerosis.

Claudia Pitzer, Carola Krüger, Christian Plaas, Friederike Kirsch, Tanjew Dittgen, Ralph Müller, Rico Laage, Stefan Kastner, Stefanie Suess, Robert Spoelgen and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Brain : a journal of neurology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

  1. Pooled it
  2. Neuroprotective therapy using granulocyte colony-stimulating factor for acute spinal cord injury: a phase I/IIa clinical trial.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2012
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3 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

15 authors at 3 institutions in 1 country.

Claudia PitzerSygnis Bioscience, Heidelberg, Germany.
Carola Krüger
Christian Plaas
Friederike Kirsch
Tanjew Dittgen
Ralph Müller
Rico Laage
Stefan Kastner
Stefanie Suess
Robert Spoelgen
Alexandre Henriques
Hannelore Ehrenreich
Wolf-Rüdiger Schäbitz
Alfred Bach
Armin Schneider
Max Planck Institute of Experimental Medicine · DEUniversity of Münster · DEExpedeon (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that results in progressive loss of motoneurons, motor weakness and death within 1-5 years after disease onset. Therapeutic options remain limited despite a substantial number of approaches that have been tested clinically. In particular, various neurotrophic factors have been investigated. Failure in these trials has been largely ascribed to problems of insufficient dosing or inability to cross the blood-brain barrier (BBB). We have recently uncovered the neurotrophic properties of the haematopoietic protein granulocyte-colony stimulating factor (G-CSF). The protein is clinically well tolerated and crosses the intact BBB. This study examined the potential role of G-CSF in motoneuron diseases. We investigated the expression of the G-CSF receptor in motoneurons and studied effects of G-CSF in a motoneuron cell line and in the SOD1(G93A) transgenic mouse model. The neurotrophic growth factor was applied both by continuous subcutaneous delivery and CNS-targeted transgenic overexpression. This study shows that given at the stage of the disease where muscle denervation is already evident, G-CSF leads to significant improvement in motor performance, delays the onset of severe motor impairment and prolongs overall survival of SOD1(G93A)tg mice. The G-CSF receptor is expressed by motoneurons and G-CSF protects cultured motoneuronal cells from apoptosis. In ALS mice, G-CSF increased survival of motoneurons and decreased muscular denervation atrophy. We conclude that G-CSF is a novel neurotrophic factor for motoneurons that is an attractive and feasible drug candidate for the treatment of ALS.

Indexed as

Amyotrophic Lateral SclerosisAnimalsApoptosisCells, CulturedDisease Models, AnimalDisease ProgressionDrug Evaluation, PreclinicalFemaleFilgrastimGranulocyte Colony-Stimulating FactorHumansInfusions, SubcutaneousMiceMice, Inbred C57BLMice, TransgenicMotor NeuronsFilgrastimGranulocyte Colony-Stimulating FactorReceptors, Granulocyte Colony-Stimulating FactorRecombinant ProteinsSOD1 protein, humanSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1

Identifiers

PMID18835867
PMCPMC2639207
OpenAlexW2115856407

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.