Evidence map›Paper›PMID 38697975›Full record

ArticleNature communications2024

Disease related changes in ATAC-seq of iPSC-derived motor neuron lines from ALS patients and controls.

Stanislav Tsitkov, Kelsey Valentine, Velina Kozareva, Aneesh Donde, Aaron Frank, Susan Lei, Answer ALS Consortium, Jennifer E Van Eyk, Steve Finkbeiner, Jeffrey D Rothstein and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Wild-typemedRxiv : the preprint server for health sciences · 2026
    Article
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  4. Review
  5. Article
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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

14 authors.

Stanislav TsitkovDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Kelsey ValentineDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Velina KozarevaDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Aneesh DondeDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Aaron FrankCedars-Sinai Biomanufacturing Center, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Susan LeiCedars-Sinai Biomanufacturing Center, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Answer ALS Consortium
Jennifer E Van EykAdvanced Clinical Biosystems Research Institute, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0001-9050-148X
Steve FinkbeinerCenter for Systems and Therapeutics, Gladstone Institutes, San Francisco, CA, USA.
Jeffrey D RothsteinBrain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Leslie M ThompsonDepartment of Neurobiology and Behavior, University of California, Irvine, CA, USA.
Dhruv SareenCedars-Sinai Biomanufacturing Center, Cedars-Sinai Medical Center, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-0898-9656
Clive N SvendsenThe Board of Governors Regenerative Medicine Institute and Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0001-8696-3446
Ernest FraenkelDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA. fraenkel-admin@mit.edu.ORCID http://orcid.org/0000-0001-9249-8181

Funding

Integrative Multi-Omic Discovery of Proximal Mechanisms Driving Age-Dependent NeurodegenerationRF1AG057331 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI FEANY, MEL B, FRAENKEL, ERNEST · 2017 to 2017
$4.8M
NIA NIH HHS RF1 AG057331
6 · The paper itself

Abstract

Amyotrophic Lateral Sclerosis (ALS), like many other neurodegenerative diseases, is highly heritable, but with only a small fraction of cases explained by monogenic disease alleles. To better understand sporadic ALS, we report epigenomic profiles, as measured by ATAC-seq, of motor neuron cultures derived from a diverse group of 380 ALS patients and 80 healthy controls. We find that chromatin accessibility is heavily influenced by sex, the iPSC cell type of origin, ancestry, and the inherent variance arising from sequencing. Once these covariates are corrected for, we are able to identify ALS-specific signals in the data. Additionally, we find that the ATAC-seq data is able to predict ALS disease progression rates with similar accuracy to methods based on biomarkers and clinical status. These results suggest that iPSC-derived motor neurons recapitulate important disease-relevant epigenomic changes.

Indexed as

Amyotrophic Lateral SclerosisInduced Pluripotent Stem CellsMotor NeuronsAgedCase-Control StudiesChromatinChromatin Immunoprecipitation SequencingDisease ProgressionEpigenesis, GeneticEpigenomicsFemaleHumansMaleMiddle AgedChromatin

Identifiers

PMID38697975
PMCPMC11066062

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.