Evidence map›Paper›PMID 32065260›Full record

ArticleActa neuropathologica2020

Synaptotagmin 13 is neuroprotective across motor neuron diseases.

M Nizzardo, M Taiana, F Rizzo, J Aguila Benitez, J Nijssen, I Allodi, V Melzi, N Bresolin, G P Comi, E Hedlund and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Acta neuropathologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 3 pooled it
2.9field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 3 syntheses or guidelines pooled it, 55 citations in OpenAlex.

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  18. Role of synaptotagmin 13 (SYT13) in promoting breast cancer and signaling pathways.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

M NizzardoDino Ferrari Centre, Neuroscience Section, Department of Pathophysiology and Transplantation (DEPT), University of Milan, Milan, Italy.
M TaianaDino Ferrari Centre, Neuroscience Section, Department of Pathophysiology and Transplantation (DEPT), University of Milan, Milan, Italy.
F RizzoDino Ferrari Centre, Neuroscience Section, Department of Pathophysiology and Transplantation (DEPT), University of Milan, Milan, Italy.
J Aguila BenitezDepartment of Neuroscience, Biomedicum D7, Karolinska Institutet, Solna v. 9, 171 77, Stockholm, Sweden.
J NijssenDepartment of Neuroscience, Biomedicum D7, Karolinska Institutet, Solna v. 9, 171 77, Stockholm, Sweden.
I AllodiDepartment of Neuroscience, Biomedicum D7, Karolinska Institutet, Solna v. 9, 171 77, Stockholm, Sweden.
V MelziDino Ferrari Centre, Neuroscience Section, Department of Pathophysiology and Transplantation (DEPT), University of Milan, Milan, Italy.
N BresolinDino Ferrari Centre, Neuroscience Section, Department of Pathophysiology and Transplantation (DEPT), University of Milan, Milan, Italy.
G P ComiDino Ferrari Centre, Neuroscience Section, Department of Pathophysiology and Transplantation (DEPT), University of Milan, Milan, Italy.
E HedlundDepartment of Neuroscience, Biomedicum D7, Karolinska Institutet, Solna v. 9, 171 77, Stockholm, Sweden. eva.hedlund@ki.se.
S CortiDino Ferrari Centre, Neuroscience Section, Department of Pathophysiology and Transplantation (DEPT), University of Milan, Milan, Italy. stefania.corti@unimi.it.ORCID 0000-0001-5425-969X
University of Milan · ITKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA), spinal and lower brainstem motor neurons degenerate, but some motor neuron subtypes are spared, including oculomotor neurons (OMNs). The mechanisms responsible for this selective degeneration are largely unknown, but the molecular signatures of resistant and vulnerable motor neurons are distinct and offer clues to neuronal resilience and susceptibility. Here, we demonstrate that healthy OMNs preferentially express Synaptotagmin 13 (SYT13) compared to spinal motor neurons. In end-stage ALS patients, SYT13 is enriched in both OMNs and the remaining relatively resilient spinal motor neurons compared to controls. Overexpression of SYT13 in ALS and SMA patient motor neurons in vitro improves their survival and increases axon lengths. Gene therapy with Syt13 prolongs the lifespan of ALS mice by 14% and SMA mice by 50% by preserving motor neurons and delaying muscle denervation. SYT13 decreases endoplasmic reticulum stress and apoptosis of motor neurons, both in vitro and in vivo. Thus, SYT13 is a resilience factor that can protect motor neurons and a candidate therapeutic target across motor neuron diseases.

Indexed as

Amyotrophic Lateral SclerosisAnimalsDisease Models, AnimalFemaleHumansMaleMiceMice, TransgenicMotor Neuron DiseaseMotor NeuronsSuperoxide DismutaseSynaptotagminsSuperoxide DismutaseSynaptotagminsSYT13 protein, human

Identifiers

PMID32065260
PMCPMC7181443
OpenAlexW3006384260

What OpenQuestion holds

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Registered trials

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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.