Evidence map›Paper›PMID 31300041›Full record

ArticleActa neuropathologica communications2019

Reduction of ephrin-A5 aggravates disease progression in amyotrophic lateral sclerosis.

Laura Rué, Patrick Oeckl, Mieke Timmers, Annette Lenaerts, Jasmijn van der Vos, Silke Smolders, Lindsay Poppe, Antina de Boer, Ludo Van Den Bosch, Philip Van Damme and 5 more

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Metallothionein and neurodegenerative diseases.Neural regeneration research · 2026
    Article
  2. Review
  3. Article
  4. Plasma proteomic analysis identifies proteins and pathways related to Alzheimer's risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  5. Article
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  7. Article
  8. Article
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  10. Review
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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

15 authors.

Laura RuéDepartment of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), KU Leuven - University of Leuven, Leuven, Belgium.ORCID 0000-0001-5415-5153
Patrick OecklDepartment of Neurology, Ulm University Hospital, Ulm, Germany.
Mieke TimmersDepartment of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), KU Leuven - University of Leuven, Leuven, Belgium.
Annette LenaertsDepartment of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), KU Leuven - University of Leuven, Leuven, Belgium.
Jasmijn van der VosDepartment of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), KU Leuven - University of Leuven, Leuven, Belgium.
Silke SmoldersDepartment of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), KU Leuven - University of Leuven, Leuven, Belgium.
Lindsay PoppeDepartment of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), KU Leuven - University of Leuven, Leuven, Belgium.
Antina de BoerDepartment of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), KU Leuven - University of Leuven, Leuven, Belgium.
Ludo Van Den BoschDepartment of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), KU Leuven - University of Leuven, Leuven, Belgium.
Philip Van DammeDepartment of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), KU Leuven - University of Leuven, Leuven, Belgium.
Jochen H WeishauptDepartment of Neurology, Ulm University Hospital, Ulm, Germany.
Albert C LudolphDepartment of Neurology, Ulm University Hospital, Ulm, Germany.
Markus OttoDepartment of Neurology, Ulm University Hospital, Ulm, Germany.
Wim RobberechtDepartment of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), KU Leuven - University of Leuven, Leuven, Belgium.
Robin LemmensDepartment of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), KU Leuven - University of Leuven, Leuven, Belgium. robin.lemmens@uzleuven.be.

Funding

ALS Association 039CYKALS Association noneALS League Belgium noneCSL Behring noneEen Hart voor ALS noneEU Joint Programme - Neurodegenerative Disease Research (JPND) network, PreFrontAls 01ED1512European Research Council (ERC) 340429Foundation of the state of Baden-Württemberg D.3830Fund for Scientific Research Flanders 1136917NFund for Scientific Research Flanders G.0996.14NGeneeskundige Stichting Koningin Elisabeth (G.S.K.E.) noneGerman Federal Ministry of Education and Research FTLDc 01GI007A, MND-Net 01GI0704Laevers Fund for ALS Research noneOpening the Future noneThierry Latran Foundation D.5009Thierry Latran Foundation FTL AAP2013VIB none
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that affects motor neurons in the brainstem, spinal cord and motor cortex. ALS is characterized by genetic and clinical heterogeneity, suggesting the existence of genetic factors that modify the phenotypic expression of the disease. We previously identified the axonal guidance EphA4 receptor, member of the Eph-ephrin system, as an ALS disease-modifying factor. EphA4 genetic inhibition rescued the motor neuron phenotype in zebrafish and a rodent model of ALS. Preventing ligands from binding to the EphA4 receptor also successfully improved disease, suggesting a role for EphA4 ligands in ALS. One particular ligand, ephrin-A5, is upregulated in reactive astrocytes after acute neuronal injury and inhibits axonal regeneration. Moreover, it plays a role during development in the correct pathfinding of motor axons towards their target limb muscles. We hypothesized that a constitutive reduction of ephrin-A5 signalling would benefit disease progression in a rodent model for ALS. We discovered that in the spinal cord of control and symptomatic ALS mice ephrin-A5 was predominantly expressed in neurons. Surprisingly, reduction of ephrin-A5 levels in SOD1

Indexed as

Disease ProgressionAdultAgedAmyotrophic Lateral SclerosisAnimalsEphrin-A5FemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMiddle AgedSuperoxide Dismutase-1Ephrin-A5SOD1 protein, humanSuperoxide Dismutase-1Amyotrophic lateral sclerosisEphA4Ephrin-A5Motor neuronNeurodegenerationSOD1G93A

Identifiers

PMID31300041
PMCPMC6626434

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.