Evidence map›Paper›PMID 31661035›Full record

ArticleActa neuropathologica communications2019

Sarm1 deletion suppresses TDP-43-linked motor neuron degeneration and cortical spine loss.

Matthew A White, Ziqiang Lin, Eugene Kim, Christopher M Henstridge, Emiliano Pena Altamira, Camille K Hunt, Ella Burchill, Isobel Callaghan, Andrea Loreto, Heledd Brown-Wright and 5 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
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  6. Caspase-3 cleaves and activates the NADase SARM1 to promote apoptosis, linking two cell death mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  16. Regulation of TIR-1/SARM-1 by miR-71 Protects Dopaminergic Neurons in aInternational journal of molecular sciences · 2024
    Article
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  18. Review
  19. Loss of SARM1 ameliorates secondary thalamic neurodegeneration after cerebral infarction.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
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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

15 authors at 6 institutions in 2 countries.

Matthew A WhiteDepartment of Basic and Clinical Neuroscience, The Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE5 9RT, UK.
Ziqiang LinDepartment of Basic and Clinical Neuroscience, The Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE5 9RT, UK.
Eugene KimBRAIN Centre (Biomarker Research And Imaging for Neuroscience), Department of Neuroimaging, IoPPN, King's College London, London, UK.
Christopher M HenstridgeDivision of Systems Medicine, School of Medicine, University of Dundee, Dundee, Scotland, UK.
Emiliano Pena AltamiraDepartment of Basic and Clinical Neuroscience, The Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE5 9RT, UK.
Camille K HuntDepartment of Basic and Clinical Neuroscience, The Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE5 9RT, UK.
Ella BurchillDepartment of Basic and Clinical Neuroscience, The Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE5 9RT, UK.
Isobel CallaghanDepartment of Basic and Clinical Neuroscience, The Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE5 9RT, UK.
Andrea LoretoJohn van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Heledd Brown-WrightDepartment of Neuroscience, Sheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield, UK.
Richard MeadDepartment of Neuroscience, Sheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield, UK.
Camilla SimmonsBRAIN Centre (Biomarker Research And Imaging for Neuroscience), Department of Neuroimaging, IoPPN, King's College London, London, UK.
Diana CashBRAIN Centre (Biomarker Research And Imaging for Neuroscience), Department of Neuroimaging, IoPPN, King's College London, London, UK.
Michael P ColemanJohn van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Jemeen SreedharanDepartment of Basic and Clinical Neuroscience, The Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE5 9RT, UK. jemeen.sreedharan@kcl.ac.uk.ORCID 0000-0002-8682-6844
King's College London · GBWellcome Centre for Human Neuroimaging · GBUniversity of Sheffield · GBBabraham Institute · GBUniversity of Cambridge · GBUniversity of Dundee · GB

Funding

Medical Research Council MR/K010611/1Motor Neurone Disease Association SITRAN/APR13/983-797Motor Neurone Disease Association Sreedharan/Jan13/943-795Motor Neurone Disease Association SREEDHARAN/JAN13/943-795Parkinson's UK G-1602Wellcome Trust 210904/Z/18/Z
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative condition that primarily affects the motor system and shares many features with frontotemporal dementia (FTD). Evidence suggests that ALS is a 'dying-back' disease, with peripheral denervation and axonal degeneration occurring before loss of motor neuron cell bodies. Distal to a nerve injury, a similar pattern of axonal degeneration can be seen, which is mediated by an active axon destruction mechanism called Wallerian degeneration. Sterile alpha and TIR motif-containing 1 (Sarm1) is a key gene in the Wallerian pathway and its deletion provides long-term protection against both Wallerian degeneration and Wallerian-like, non-injury induced axonopathy, a retrograde degenerative process that occurs in many neurodegenerative diseases where axonal transport is impaired. Here, we explored whether Sarm1 signalling could be a therapeutic target for ALS by deleting Sarm1 from a mouse model of ALS-FTD, a TDP-43

Indexed as

Amyotrophic Lateral SclerosisAnimalsArmadillo Domain ProteinsCytoskeletal ProteinsDendritic SpinesFemaleFrontotemporal DementiaMaleMice, Inbred C57BLMice, KnockoutMotor CortexMotor NeuronsNeuromuscular JunctionSignal TransductionWallerian DegenerationArmadillo Domain ProteinsCytoskeletal ProteinsSARM1 protein, mouseAmyotrophic lateral sclerosisAxonal protectionDendritic spinesSterile alpha and TIR motif-containing protein 1TAR DNA-binding protein 43Wallerian degeneration

Identifiers

PMID31661035
PMCPMC6819591
OpenAlexW2981440322

What OpenQuestion holds

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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 OpenQuestion graph.