Evidence map›Paper›PMID 37577713›Full record

ArticlebioRxiv : the preprint server for biology2023

Patient iPSC models reveal glia-intrinsic phenotypes in multiple sclerosis.

Benjamin L L Clayton, Lilianne Barbar, Maria Sapar, Tomasz Rusielewicz, Kriti Kalpana, Bianca Migliori, NYSCF Global Stem Cell Array® Team, Daniel Paull, Katie Brenner, Dorota Moroziewicz and 4 more

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed, 8 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Benjamin L L ClaytonDepartment of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106, USA.
Lilianne BarbarThe New York Stem Cell Foundation Research Institute, New York, NY 10019, USA.
Maria SaparThe New York Stem Cell Foundation Research Institute, New York, NY 10019, USA.
Tomasz RusielewiczThe New York Stem Cell Foundation Research Institute, New York, NY 10019, USA.
Kriti KalpanaThe New York Stem Cell Foundation Research Institute, New York, NY 10019, USA.
Bianca MiglioriThe New York Stem Cell Foundation Research Institute, New York, NY 10019, USA.
NYSCF Global Stem Cell Array® Team
Daniel PaullThe New York Stem Cell Foundation Research Institute, New York, NY 10019, USA.
Katie BrennerThe New York Stem Cell Foundation Research Institute, New York, NY 10019, USA.
Dorota MoroziewiczThe New York Stem Cell Foundation Research Institute, New York, NY 10019, USA.
Ilana Katz SandCorinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10129, USA.
Patrizia CasacciaAdvanced Science Research Center at CUNY, New York, NY 10031, USA.
Paul J TesarDepartment of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106, USA.
Valentina FossatiThe New York Stem Cell Foundation Research Institute, New York, NY 10019, USA.
New York Stem Cell Foundation · USThe Graduate Center, CUNY · USUniversity School · USWashington University in St. Louis · US

Funding

Environmental Biosensors in the Oligodendrocyte LineageR35NS111604 · NINDS · ADVANCED SCIENCE RESEARCH CENTER · PI Patrizia Casaccia · 2019 to 2026
$9.1M
Modulating Glial Fate and Function in Development and DiseaseR35NS116842 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI Paul Joseph Tesar · 2020 to 2026
$5.3M
NINDS NIH HHS R35 NS111604NINDS NIH HHS R35 NS116842
6 · The paper itself

Abstract

Multiple sclerosis (MS) is considered an inflammatory and neurodegenerative disease of the central nervous system, typically resulting in significant neurological disability that worsens over time. While considerable progress has been made in defining the immune system's role in MS pathophysiology, the contribution of intrinsic CNS-cell dysfunction remains unclear. Here, we generated the largest reported collection of iPSC lines from people with MS spanning diverse clinical subtypes and differentiated them into glia-enriched cultures. Using single-cell transcriptomic profiling, we observed several distinguishing characteristics of MS cultures pointing to glia-intrinsic disease mechanisms. We found that iPSC-derived cultures from people with primary progressive MS contained fewer oligodendrocytes. Moreover, iPSC-oligodendrocyte lineage cells and astrocytes from people with MS showed increased expression of immune and inflammatory genes that match those of glial cells from MS postmortem brains. Thus, iPSC-derived MS models provide a unique platform for dissecting glial contributions to disease phenotypes independent of the peripheral immune system and identify potential glia-specific targets for therapeutic intervention.

Identifiers

PMID37577713
PMCPMC10418164
OpenAlexW4385494841

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.