Evidence map›Paper›PMID 29244098›Full record

ArticleBrain : a journal of neurology2018

Clemastine rescues myelination defects and promotes functional recovery in hypoxic brain injury.

Bruce A C Cree, Jianqin Niu, Kimberly K Hoi, Chao Zhao, Scott D Caganap, Roland G Henry, Dang Q Dao, Daniel R Zollinger, Feng Mei, Yun-An A Shen and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Brain : a journal of neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
11.0field-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

80 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
  2. Beyond Histamine Blockade: Clemastine Fumarate as a Promoter of Myelin Regeneration, Inflammatory Regulation, and Neuroimmune Modulation in CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
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  18. Long-Term Excessive Alcohol Consumption Enhances Myelination in the Mouse Nucleus Accumbens.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  19. Article
  20. Review

20 more citing papers are in PubMed but not listed here.

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 3 institutions in 3 countries.

Bruce A C CreeUCSF Weill Institute for Neurosciences, Department of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Jianqin NiuDepartment of Pediatrics, University of California at San Francisco, San Francisco, CA 94158, USA.
Kimberly K HoiDepartment of Pediatrics, University of California at San Francisco, San Francisco, CA 94158, USA.
Chao ZhaoWellcome Trust-Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AH, UK.
Scott D CaganapUCSF Weill Institute for Neurosciences, Department of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Roland G HenryUCSF Weill Institute for Neurosciences, Department of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Dang Q DaoDepartment of Ophthalmology, University of California at San Francisco, San Francisco, CA 94158, USA.
Daniel R ZollingerDepartment of Pediatrics, University of California at San Francisco, San Francisco, CA 94158, USA.
Feng MeiDepartment of Histology and Embryology, Collaborative Innovation Center for Brain Research, Third Military Medical University, Chongqing 400038, China.
Yun-An A ShenUCSF Weill Institute for Neurosciences, Department of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Robin J M FranklinWellcome Trust-Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AH, UK.
Erik M UllianDepartment of Ophthalmology, University of California at San Francisco, San Francisco, CA 94158, USA.
Lan XiaoDepartment of Histology and Embryology, Collaborative Innovation Center for Brain Research, Third Military Medical University, Chongqing 400038, China.
Jonah R ChanUCSF Weill Institute for Neurosciences, Department of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
Stephen P J FancyUCSF Weill Institute for Neurosciences, Department of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.
University of California, San Francisco · USArmy Medical University · CNWellcome/MRC Cambridge Stem Cell Institute · GB

Funding

Regulation of Cellular Pathwaysin Human Brain DevelopmentP01NS083513 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ALVAREZ-BUYLLA, ARTURO · 2014 to 2024
$12.6M
PREDOCTORAL TRAINING IN BIOMEDICAL SCIENCEST32GM008568 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ANSEL, KARL MARK · 1995 to 2019
$6.3M
Vasculature provides the substrate for oligodendrocyte progenitor migration in development and diseaseR01NS097551 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FANCY, STEPHEN PHILIP JAMES · 2017 to 2021
$1.7M
Medical Research Council MC_PC_12009NIGMS NIH HHS T32 GM008568NINDS NIH HHS P01 NS083513NINDS NIH HHS R01 NS097551
6 · The paper itself

Abstract

Hypoxia can injure brain white matter tracts, comprised of axons and myelinating oligodendrocytes, leading to cerebral palsy in neonates and delayed post-hypoxic leukoencephalopathy (DPHL) in adults. In these conditions, white matter injury can be followed by myelin regeneration, but myelination often fails and is a significant contributor to fixed demyelinated lesions, with ensuing permanent neurological injury. Non-myelinating oligodendrocyte precursor cells are often found in lesions in plentiful numbers, but fail to mature, suggesting oligodendrocyte precursor cell differentiation arrest as a critical contributor to failed myelination in hypoxia. We report a case of an adult patient who developed the rare condition DPHL and made a nearly complete recovery in the setting of treatment with clemastine, a widely available antihistamine that in preclinical models promotes oligodendrocyte precursor cell differentiation. This suggested possible therapeutic benefit in the more clinically prevalent hypoxic injury of newborns, and we demonstrate in murine neonatal hypoxic injury that clemastine dramatically promotes oligodendrocyte precursor cell differentiation, myelination, and improves functional recovery. We show that its effect in hypoxia is oligodendroglial specific via an effect on the M1 muscarinic receptor on oligodendrocyte precursor cells. We propose clemastine as a potential therapy for hypoxic brain injuries associated with white matter injury and oligodendrocyte precursor cell maturation arrest.

Indexed as

Action PotentialsAnimalsAnimals, NewbornCell DifferentiationCells, CulturedCerebellumClemastineDemyelinating DiseasesDisease Models, AnimalGene Expression Regulation, DevelopmentalHistamine H1 AntagonistsHumansHypoxia, BrainMaleMiceMice, KnockoutClemastineHistamine H1 AntagonistsOxygenReceptor, Muscarinic M1cerebral palsyclemastinehypoxiamyelinationoligodendrocyte

Identifiers

PMID29244098
PMCPMC6394402
OpenAlexW2772079728

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.