Evidence map›Paper›PMID 31646358›Full record

ArticleCellular and molecular life sciences : CMLS2020

Running and swimming prevent the deregulation of the BDNF/TrkB neurotrophic signalling at the neuromuscular junction in mice with amyotrophic lateral sclerosis.

Laia Just-Borràs, Erica Hurtado, Víctor Cilleros-Mañé, Olivier Biondi, Frédéric Charbonnier, Marta Tomàs, Neus Garcia, Josep Tomàs, Maria A Lanuza

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.1field-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

31 citing papers in PubMed, 42 citations in OpenAlex.

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  4. Disruption of BDNF signalling in neuropathologies.Biochemical Society transactions · 2026
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  8. Brain-derived neurotrophic factor drives muscle adaptation similar to aerobic training in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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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

9 authors at 2 institutions in 2 countries.

Laia Just-BorràsUnitat d'Histologia i Neurobiologia (UHNEUROB), Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili. Sant Llorenç 21, 43201, Reus, Spain.ORCID http://orcid.org/0000-0003-0473-3730
Erica HurtadoUnitat d'Histologia i Neurobiologia (UHNEUROB), Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili. Sant Llorenç 21, 43201, Reus, Spain.ORCID http://orcid.org/0000-0001-8930-4462
Víctor Cilleros-MañéUnitat d'Histologia i Neurobiologia (UHNEUROB), Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili. Sant Llorenç 21, 43201, Reus, Spain.ORCID http://orcid.org/0000-0001-5690-9932
Olivier BiondiUMR-S1124, INSERM, Faculté des Sciences Fondamentales et Biomédicales, Université Paris Descartes, 45 Rue des Saints-Pères, 75006, Paris, France.ORCID http://orcid.org/0000-0003-4302-6035
Frédéric CharbonnierUMR-S1124, INSERM, Faculté des Sciences Fondamentales et Biomédicales, Université Paris Descartes, 45 Rue des Saints-Pères, 75006, Paris, France.ORCID http://orcid.org/0000-0003-4341-3246
Marta TomàsUnitat d'Histologia i Neurobiologia (UHNEUROB), Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili. Sant Llorenç 21, 43201, Reus, Spain.ORCID http://orcid.org/0000-0002-4151-1697
Neus GarciaUnitat d'Histologia i Neurobiologia (UHNEUROB), Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili. Sant Llorenç 21, 43201, Reus, Spain.ORCID http://orcid.org/0000-0002-3401-8335
Josep TomàsUnitat d'Histologia i Neurobiologia (UHNEUROB), Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili. Sant Llorenç 21, 43201, Reus, Spain. josepmaria.tomas@urv.cat.ORCID http://orcid.org/0000-0002-0406-0006
Maria A LanuzaUnitat d'Histologia i Neurobiologia (UHNEUROB), Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili. Sant Llorenç 21, 43201, Reus, Spain. mariaangel.lanuza@urv.cat.ORCID http://orcid.org/0000-0003-4795-4103
Universitat Rovira i Virgili · ESDélégation Paris 5 · FR

Funding

Departament d'Universitats, Recerca i Societat de la Informació 2014SGR344Departament d'Universitats, Recerca i Societat de la Informació 2017SGR704Ministerio de Economía, Industria y Competitividad, Gobierno de España SAF2015-67143-PUniversitat Rovira i Virgili 2014PFR-URV-B2-83Universitat Rovira i Virgili 2017PFR-URV-B2-85
6 · The paper itself

Abstract

Nerve-induced muscle contraction regulates the BDNF/TrkB neurotrophic signalling to retrogradely modulate neurotransmission and protect the neuromuscular junctions and motoneurons. In muscles with amyotrophic lateral sclerosis, this pathway is strongly misbalanced and neuromuscular junctions are destabilized, which may directly cause the motoneuron degeneration and muscular atrophy observed in this disease. Here, we sought to demonstrate (1) that physical exercise, whose recommendation has been controversial in amyotrophic lateral sclerosis, would be a good option for its therapy, because it normalizes and improves the altered neurotrophin pathway and (2) a plausible molecular mechanism underlying its positive effect. SOD1-G93A mice were trained following either running or swimming-based protocols since the beginning of the symptomatic phase (day 70 of age) until day 115. Next, the full BDNF pathway, including receptors, downstream kinases and proteins related with neurotransmission, was characterized and motoneuron survival was analysed. The results establish that amyotrophic lateral sclerosis-induced damaging molecular changes in the BDNF/TrkB pathway are reduced, prevented or even overcompensated by precisely defined exercise protocols that modulate TrkB isoforms and neurotransmission regulatory proteins and reduce motoneuron death. Altogether, the maintenance of the BDNF/TrkB signalling and the downstream pathway, particularly after the swimming protocol, adds new molecular evidence of the benefits of physical exercise to reduce the impact of amyotrophic lateral sclerosis. These results are encouraging since they reveal an improvement even starting the therapy after the onset of the disease.

Indexed as

Physical Conditioning, AnimalSignal TransductionSwimmingAmyotrophic Lateral SclerosisAnimalsBrain-Derived Neurotrophic FactorDisease Models, AnimalFemaleMaleMembrane GlycoproteinsMiceMice, TransgenicMotor NeuronsMuscle, SkeletalNeuromuscular JunctionPolymorphism, Single NucleotideBrain-Derived Neurotrophic FactorMembrane GlycoproteinsNtrk2 protein, mouseProtein IsoformsProtein Kinase C-alphaProtein-Tyrosine KinasesReceptor, trkBSNARE ProteinsSod1 protein, mouseSuperoxide Dismutase-1ALSExerciseMotoneuron lossNeurotransmissionNMJSkeletal muscle

Identifiers

PMID31646358
PMCPMC11104938
OpenAlexW2981671049

What OpenQuestion holds

Textmetadata
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.