Evidence map›Paper›PMID 38559020›Full record

ArticlebioRxiv : the preprint server for biology2024

Boosting BDNF in muscle rescues impaired axonal transport in a mouse model of DI-CMTC peripheral neuropathy.

Elena R Rhymes, Rebecca L Simkin, Ji Qu, David Villarroel-Campos, Sunaina Surana, Yao Tong, Ryan Shapiro, Robert W Burgess, Xiang-Lei Yang, Giampietro Schiavo and 1 more

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

Elena R RhymesDepartment of Neuromuscular Diseases and UCL Queen Square Motor Neuron Disease Centre, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
Rebecca L SimkinDepartment of Neuromuscular Diseases and UCL Queen Square Motor Neuron Disease Centre, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.ORCID 0000-0001-8093-2139
Ji QuDepartment of Neuromuscular Diseases and UCL Queen Square Motor Neuron Disease Centre, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.ORCID 0009-0004-2225-9467
David Villarroel-CamposDepartment of Neuromuscular Diseases and UCL Queen Square Motor Neuron Disease Centre, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.ORCID 0000-0003-4250-7216
Sunaina SuranaDepartment of Neuromuscular Diseases and UCL Queen Square Motor Neuron Disease Centre, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.ORCID 0000-0002-7017-3105
Yao TongDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.
Ryan ShapiroDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.
Robert W BurgessThe Jackson Laboratory, Bar Harbor, ME 04609, USA.ORCID 0000-0002-9229-3407
Xiang-Lei YangDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.ORCID 0000-0003-2554-084X
Giampietro SchiavoDepartment of Neuromuscular Diseases and UCL Queen Square Motor Neuron Disease Centre, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.ORCID 0000-0002-4319-8745
James N SleighDepartment of Neuromuscular Diseases and UCL Queen Square Motor Neuron Disease Centre, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.ORCID 0000-0002-3782-9045
UK Dementia Research Institute · GBNational Hospital for Neurology and Neurosurgery · GBScripps Research Institute · USJackson Laboratory · US

Funding

Link extracellular function of tRNA synthetase with pathological mechanism of diseaseR35GM139627 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI YANG, XIANG-LEI · 2021 to 2025
$2.3M
Medical Research Council MR/S006990/1NIGMS NIH HHS R35 GM139627Wellcome Trust
6 · The paper itself

Abstract

Charcot-Marie-Tooth disease (CMT) is a genetic peripheral neuropathy caused by mutations in many functionally diverse genes. The aminoacyl-tRNA synthetase (ARS) enzymes, which transfer amino acids to partner tRNAs for protein synthesis, represent the largest protein family genetically linked to CMT aetiology, suggesting pathomechanistic commonalities. Dominant intermediate CMT type C (DI-CMTC) is caused by

Indexed as

aminoacyl-tRNA synthetase (ARS)Charcot-Marie-Tooth disease (CMT)intravital imaging, motor neuronneuromuscular junction (NMJ)neurotrophic factorsneurotrophinsperipheral neuropathyTrk receptorsYARS1

Identifiers

PMID38559020
PMCPMC10979848
OpenAlexW4362735524

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.