Evidence map›Paper›PMID 42567160›Full record

ArticleNeuron2026

Temporal changes in metabolism guide oligodendrocyte precursor cell dynamics in aging and multiple sclerosis.

Tess Dierckx, Sarah E Wilson, Rebecca Buchanan, Themistoklis M Tsarouchas, Yuhsiang Cheng, Maria Sacconi Nunez, Kelly Strickland, Dena Kumsa, Yohan S S Auguste, Sam Vanherle and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuron, 2026. 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.

No citing paper in PubMed yet.

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

19 authors.

Tess DierckxDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA.
Sarah E WilsonDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA; Stem Cell Biology and Regenerative Medicine Graduate Program, Stanford University, Palo Alto, CA 94305, USA.
Rebecca BuchananDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA.
Themistoklis M TsarouchasDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA.
Yuhsiang ChengDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA; Neurosciences Interdepartmental Graduate Program, Stanford University, Palo Alto, CA 94305, USA.
Maria Sacconi NunezDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA.
Kelly StricklandDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA.
Dena KumsaDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA.
Yohan S S AugusteDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA; Neurosciences Interdepartmental Graduate Program, Stanford University, Palo Alto, CA 94305, USA.
Sam VanherleDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium; University MS Center Hasselt, 3900 Pelt, Belgium.
Sander BouwmanDepartment of Biomedical Sciences, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Daniela RojoDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA.
Louisa Dal CengioDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA.
Celia Lerma-MartinDepartment of Neurology, Division of Neuroimmunology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Yassene MohammedCenter for Proteomics and Metabolomics, Leiden University Medical Center, Leiden, the Netherlands.
Lucas SchirmerDepartment of Neurology, Division of Neuroimmunology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany; Mannheim Center for Translational Neuroscience and Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany; Interdisciplinary Center for Neurosciences, Heidelberg University, Heidelberg, Germany.
Jeroen F J BogieDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium; University MS Center Hasselt, 3900 Pelt, Belgium.
Bart J L EggenDepartment of Biomedical Sciences, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands; MS Centrum Noord Nederland, Groningen, the Netherlands.
Erin M GibsonDepartment of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Electronic address: egibson1@stanford.edu.

Funding

Circadian mechanisms of myelinationR01NS126610 · NINDS · STANFORD UNIVERSITY · PI Erin G Valdez · 2023 to 2026
$1.9M
NINDS NIH HHS R01 NS126610
6 · The paper itself

Abstract

Impaired oligodendrocyte precursor cell (OPC) differentiation limits myelin renewal in aging and contributes to multiple sclerosis (MS) progression. How aging drives OPC deficits remains incompletely understood. We find dysregulation of genes associated with the circadian clock, including Bmal1, and metabolism in aged compared with young OPCs. Targeted loss of Bmal1 in OPCs drives metabolic dysfunction, leading to cellular senescence and impaired dynamics. OPC proliferation and differentiation occur at different rates throughout the day in young adult mice and become disrupted with aging. Chronotherapeutic targeting of BMAL1-controlled sirtuin signaling restores Bmal1-disrupted OPC dynamics after demyelination via sirtuin 2 (Sirt2)-dependent mechanisms. Induced pluripotent stem cell (iPSC)-derived OPCs from MS patients and MS lesion oligodendroglia recapitulate BMAL1 and SIRT2 disruptions. These findings establish BMAL1 as a key regulator of OPC energy metabolism, sirtuin homeostasis, and senescence. We anticipate that this work will provide a foundation for future studies investigating the interconnected roles of aging, circadian disruption, and myelin biology.

Indexed as

agingBMAL1circadianiPSCmetabolismmultiple sclerosismyelinationoligodendrocyte precursor cellsoligodendrocytesOPCs

Identifiers

PMID42567160
PMCPMC13482912

What OpenQuestion 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 OpenQuestion graph.