Evidence map›Paper›PMID 31817487›Full record

ReviewCells2019

The Impact of Kinases in Amyotrophic Lateral Sclerosis at the Neuromuscular Synapse: Insights into BDNF/TrkB and PKC Signaling.

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

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

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  15. Role of RNA Oxidation in Neurodegenerative Diseases.International journal of molecular sciences · 2020
    Review
  16. Histone deacetylase-3: Friend and foe of the brain.Experimental biology and medicine (Maywood, N.J.) · 2020
    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

7 authors at 1 institution in 1 country.

Maria A LanuzaUnitat d'Histologia i Neurobiologia (UHNEUROB), Universitat Rovira i Virgili, Facultat de Medicina i Ciències de la Salut, Sant Llorenç 21, 43201 Reus, Spain.ORCID 0000-0003-4795-4103
Laia Just-BorràsUnitat d'Histologia i Neurobiologia (UHNEUROB), Universitat Rovira i Virgili, Facultat de Medicina i Ciències de la Salut, Sant Llorenç 21, 43201 Reus, Spain.
Erica HurtadoUnitat d'Histologia i Neurobiologia (UHNEUROB), Universitat Rovira i Virgili, Facultat de Medicina i Ciències de la Salut, Sant Llorenç 21, 43201 Reus, Spain.
Víctor Cilleros-MañéUnitat d'Histologia i Neurobiologia (UHNEUROB), Universitat Rovira i Virgili, Facultat de Medicina i Ciències de la Salut, Sant Llorenç 21, 43201 Reus, Spain.
Marta TomàsUnitat d'Histologia i Neurobiologia (UHNEUROB), Universitat Rovira i Virgili, Facultat de Medicina i Ciències de la Salut, Sant Llorenç 21, 43201 Reus, Spain.
Neus GarciaUnitat d'Histologia i Neurobiologia (UHNEUROB), Universitat Rovira i Virgili, Facultat de Medicina i Ciències de la Salut, Sant Llorenç 21, 43201 Reus, Spain.ORCID 0000-0002-3401-8335
Josep TomàsUnitat d'Histologia i Neurobiologia (UHNEUROB), Universitat Rovira i Virgili, Facultat de Medicina i Ciències de la Salut, Sant Llorenç 21, 43201 Reus, Spain.ORCID 0000-0002-0406-0006
Universitat Rovira i Virgili · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) promotes neuron survival in adulthood in the central nervous system. In the peripheral nervous system, BDNF is a contraction-inducible protein that, through its binding to tropomyosin-related kinase B receptor (TrkB), contributes to the retrograde neuroprotective control done by muscles, which is necessary for motor neuron function. BDNF/TrkB triggers downstream presynaptic pathways, involving protein kinase C, essential for synaptic function and maintenance. Undeniably, this reciprocally regulated system exemplifies the tight communication between nerve terminals and myocytes to promote synaptic function and reveals a new view about the complementary and essential role of pre and postsynaptic interplay in keeping the synapse healthy and strong. This signaling at the neuromuscular junction (NMJ) could establish new intervention targets across neuromuscular diseases characterized by deficits in presynaptic activity and muscle contractility and by the interruption of the connection between nervous and muscular tissues, such as amyotrophic lateral sclerosis (ALS). Indeed, exercise and other therapies that modulate kinases are effective at delaying ALS progression, preserving NMJs and maintaining motor function to increase the life quality of patients. Altogether, we review synaptic activity modulation of the BDNF/TrkB/PKC signaling to sustain NMJ function, its and other kinases' disturbances in ALS and physical and molecular mechanisms to delay disease progression.

Indexed as

Signal TransductionAmyotrophic Lateral SclerosisAnimalsBrain-Derived Neurotrophic FactorExerciseGene ExpressionHumansMembrane GlycoproteinsMotor NeuronsMuscle, SkeletalNeuromuscular JunctionProtein Kinase CReceptor, trkBBDNF protein, humanBrain-Derived Neurotrophic FactorMembrane GlycoproteinsProtein Kinase CReceptor, trkBtropomyosin-related kinase-B, humanALSBDNFexercisekinaseneuromuscularNMJPKCTrkB

Identifiers

PMID31817487
PMCPMC6953086
OpenAlexW2991732008

What Socratic 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 Socratic graph.