Evidence map›Paper›PMID 38413232›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2024

Human Motor Neurons Elicit Pathological Hallmarks of ALS and Reveal Potential Biomarkers of the Disease in Response to Prolonged IFNγ Exposure.

Changho Chun, Jung Hyun Lee, Mark Bothwell, Paul Nghiem, Alec S T Smith, David L Mack

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. 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

6 authors at 2 institutions in 2 countries.

Changho ChunDepartments of Bioengineering, University of Washington, Seattle, Washington 98195.
Jung Hyun LeeInstitute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington 98109.
Mark BothwellInstitute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington 98109.
Paul NghiemDepartments of Dermatology, School of Medicine, University of Washington, Seattle, Washington 98195.
Alec S T SmithInstitute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington 98109 dmack21@uw.edu astsmith@uw.edu.
David L MackDepartments of Bioengineering, University of Washington, Seattle, Washington 98195 dmack21@uw.edu astsmith@uw.edu.
University of Washington · USFred Hutch Cancer Center · US

Funding

Understand & overcome resistance to PD-1P01CA225517 · NCI · UNIVERSITY OF WASHINGTON · PI Cecilia C Yeung · 2019 to 2026
$22.7M
Using functional readouts from engineering models of innervated skeletal muscle to assess the efficacy of CRISPR-based c9orf72 ALS gene therapiesR03TR004009 · NCATS · UNIVERSITY OF WASHINGTON · PI SMITH, ALEC SIMON TULLOCH · 2022 to 2023
$177k
NCATS NIH HHS R03 TR004009NCI NIH HHS P01 CA225517
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a debilitating neurodegenerative disorder marked by progressive motor neuron degeneration and muscle denervation. A recent transcriptomic study integrating a wide range of human ALS samples revealed that the upregulation of p53, a downstream target of inflammatory stress, is commonly detected in familial and sporadic ALS cases by a mechanism linked to a transactive response DNA-binding protein 43 (TDP-43) dysfunction. In this study, we show that prolonged interferon-gamma (IFNγ) treatment of human induced pluripotent stem cell-derived spinal motor neurons results in a severe cytoplasmic aggregation of TDP-43. TDP-43 dysfunction resulting from either IFNγ exposure or an ALS-associated TDP-43 mutation was associated with the activation of the p53 pathway. This was accompanied by the hyperactivation of neuronal firing, followed by the complete loss of their electrophysiological function. Through a comparative single-cell transcriptome analysis, we have identified significant alterations in ALS-associated genes in motor neurons exposed to IFNγ, implicating their direct involvement in ALS pathology. Interestingly, IFNγ was found to induce significant levels of programmed death-ligand 1 (PD-L1) expression in motor neurons without affecting the levels of any other immune checkpoint proteins. This finding suggests a potential role of excessive PD-L1 expression in ALS development, given that PD-L1 was recently reported to impair neuronal firing ability in mice. Our findings suggest that exposing motor neurons to IFNγ could directly derive ALS pathogenesis, even without the presence of the inherent genetic mutation or functional glia component. Furthermore, this study provides a comprehensive list of potential candidate genes for future immunotherapeutic targets with which to treat sporadic forms of ALS, which account for 90% of all reported cases.

Indexed as

Amyotrophic Lateral SclerosisInduced Pluripotent Stem CellsAnimalsB7-H1 AntigenBiomarkersDNA-Binding ProteinsHumansInterferon-gammaMiceMotor NeuronsTumor Suppressor Protein p53B7-H1 AntigenBiomarkersDNA-Binding ProteinsInterferon-gammaTumor Suppressor Protein p53amyotrophic lateral sclerosisinterferon-gammaiPSC-derived spinal motor neuronneuroinflammationp53 pathwayTDP-43 proteinopathy

Identifiers

PMID38413232
PMCPMC11026347
OpenAlexW4392188915

What Socratic 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 Socratic graph.