Evidence map›Paper›PMID 26064939›Full record

ArticleBioMed research international2015

Novel Mechanisms of Spinal Cord Plasticity in a Mouse Model of Motoneuron Disease.

Rosario Gulino, Rosalba Parenti, Massimo Gulisano

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 39% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Neuroprotective role of Noggin in spinal cord injury.Neural regeneration research · 2023
    Review
  4. Synaptic Dysfunction and Plasticity in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
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

3 authors at 1 institution in 1 country.

Rosario GulinoDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 64, 95127 Catania, Italy ; IOM Ricerca s.r.l., Via Penninazzo 11, 95029 Viagrande, Italy.
Rosalba ParentiDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 64, 95127 Catania, Italy.ORCID 0000-0002-1614-4696
Massimo GulisanoDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 64, 95127 Catania, Italy.
University of Catania · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A hopeful spinal cord repairing strategy involves the activation of neural precursor cells. Unfortunately, their ability to generate neurons after injury appears limited. Another process promoting functional recovery is synaptic plasticity. We have previously studied some mechanisms of spinal plasticity involving BDNF, Shh, Notch-1, Numb, and Noggin, by using a mouse model of motoneuron depletion induced by cholera toxin-B saporin. TDP-43 is a nuclear RNA/DNA binding protein involved in amyotrophic lateral sclerosis. Interestingly, TDP-43 could be localized at the synapse and affect synaptic strength. Here, we would like to deepen the investigation of this model of spinal plasticity. After lesion, we observed a glial reaction and an activity-dependent modification of Shh, Noggin, and Numb proteins. By using multivariate regression models, we found that Shh and Noggin could affect motor performance and that these proteins could be associated with both TDP-43 and Numb. Our data suggest that TDP-43 is likely an important regulator of synaptic plasticity, probably in collaboration with other proteins involved in both neurogenesis and synaptic plasticity. Moreover, given the rapidly increasing knowledge about spinal cord plasticity, we believe that further efforts to achieve spinal cord repair by stimulating the intrinsic potential of spinal cord will produce interesting results.

Indexed as

AnimalsCarrier ProteinsCell ProliferationDisease Models, AnimalDNA-Binding ProteinsHedgehog ProteinsHumansMembrane ProteinsMiceMotor Neuron DiseaseMotor NeuronsNerve Tissue ProteinsNeuronal PlasticityNoggin ProteinRibosome Inactivating Proteins, Type 1SaporinsCarrier ProteinsDNA-Binding ProteinsHedgehog ProteinsMembrane ProteinsNerve Tissue ProteinsNoggin ProteinNumb protein, mouseRibosome Inactivating Proteins, Type 1SaporinsShh protein, mouseTardbp protein, mouse

Identifiers

PMID26064939
PMCPMC4433663
OpenAlexW2016794472

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.