Evidence map›Paper›PMID 36601738›Full record

ArticleEMBO molecular medicine2023

Synaptogenic gene therapy with FGF22 improves circuit plasticity and functional recovery following spinal cord injury.

Almir Aljović, Anne Jacobi, Maite Marcantoni, Fritz Kagerer, Kristina Loy, Arek Kendirli, Jonas Bräutigam, Luca Fabbio, Valérie Van Steenbergen, Katarzyna Pleśniar and 2 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2023. 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
3.3field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
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

12 authors at 1 institution in 1 country.

Almir Aljović *Institute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.ORCID 0000-0001-9725-6368
Anne Jacobi *Institute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.ORCID 0000-0002-8197-3554
Maite MarcantoniInstitute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.ORCID 0000-0001-6665-5251
Fritz KagererInstitute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.ORCID 0000-0002-4943-0509
Kristina LoyInstitute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.
Arek KendirliInstitute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.ORCID 0000-0001-6888-9131
Jonas BräutigamInstitute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.
Luca FabbioInstitute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.ORCID 0000-0001-7953-2162
Valérie Van SteenbergenInstitute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.ORCID 0000-0002-5836-2122
Katarzyna PleśniarInstitute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.
Martin KerschensteinerInstitute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.ORCID 0000-0003-4898-9383
Florence M BareyreInstitute of Clinical Neuroimmunology, University Hospital, LMU Munich, Munich, Germany.ORCID 0000-0002-0917-1725
LMU Klinikum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Functional recovery following incomplete spinal cord injury (SCI) depends on the rewiring of motor circuits during which supraspinal connections form new contacts onto spinal relay neurons. We have recently identified a critical role of the presynaptic organizer FGF22 for the formation of new synapses in the remodeling spinal cord. Here, we now explore whether and how targeted overexpression of FGF22 can be used to mitigate the severe functional consequences of SCI. By targeting FGF22 expression to either long propriospinal neurons, excitatory interneurons, or a broader population of interneurons, we establish that FGF22 can enhance neuronal rewiring both in a circuit-specific and comprehensive way. We can further demonstrate that the latter approach can restore functional recovery when applied either on the day of the lesion or within 24 h. Our study thus establishes viral gene transfer of FGF22 as a new synaptogenic treatment for SCI and defines a critical therapeutic window for its application.

Indexed as

Spinal Cord InjuriesFibroblast Growth FactorsHumansInterneuronsNeuronsSpinal CordSynapsesFGF22 protein, humanFibroblast Growth Factorsadeno-associated virusFGF22gene therapyrecoveryspinal cord injury

Identifiers

PMID36601738
PMCPMC9906383
OpenAlexW4313545140

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.