Loss of synaptic Munc13-1 underlies neurotransmission abnormalities in spinal muscular atrophy.

Mehri Moradi, Chunchu Deng, Michael Sendtner

Abstract read

In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing 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

1 citing paper in PubMed.

Astrocyte targeted SMN1 gene therapy and forskolin application improves astrocyte filopodia actin defects and motor neuron synaptic dysfunction in human SMA disease pathology.bioRxiv : the preprint server for biology · 2026
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

3 authors.

Mehri MoradiInstitute of Clinical Neurobiology, University Hospital Wuerzburg, Versbacher Str. 5, 97078, Wuerzburg, Germany.

Chunchu DengInstitute of Clinical Neurobiology, University Hospital Wuerzburg, Versbacher Str. 5, 97078, Wuerzburg, Germany.

Michael SendtnerInstitute of Clinical Neurobiology, University Hospital Wuerzburg, Versbacher Str. 5, 97078, Wuerzburg, Germany. Sendtner_M@ukw.de.ORCID http://orcid.org/0000-0002-4737-2974

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spinal muscular atrophy (SMA) is a devastating neurodegenerative disease characterized by degeneration of spinal motoneurons, leading to muscle atrophy and synaptic loss. SMN functions in mRNA splicing, transport, and local translation are crucial for maintaining synaptic integrity. Within the presynaptic membrane, the active zone orchestrates the docking and priming of synaptic vesicles. The Munc13 family proteins are key active zone components that operate precise neurotransmitter release in conjunction with voltage-gated Ca

Indexed as

Muscular Atrophy, SpinalNerve Tissue ProteinsSynapsesSynaptic TransmissionAnimalsAxonsCalcium ChannelsHumansMiceMotor NeuronsRNA, MessengerSurvival of Motor Neuron 1 ProteinSynaptic VesiclesCalcium ChannelsNerve Tissue ProteinsRNA, MessengerSurvival of Motor Neuron 1 ProteinUnc13a protein, mouseActive zoneAxonal mRNA localizationMunc13-2Survival of motor neuronSynapse degeneration

Identifiers

PMID40879740

DOI10.1007/s00018-025-05859-7

PMCPMC12397458

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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.