Evidence map›Paper›PMID 39125778›Full record

ArticleInternational journal of molecular sciences2024

Neuroprotective Effect of Clemastine Improved Oligodendrocyte Proliferation through the MAPK/ERK Pathway in a Neonatal Hypoxia Ischemia Rat Model.

Maria E Bernis, Charlotte Hakvoort, Efe Nacarkucuk, Hannah Burkard, Anna-Sophie Bremer, Margit Zweyer, Elke Maes, Kora A Grzelak, Hemmen Sabir

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. TRPC4 Mediates Trigeminal Neuropathic Pain via CaCNS neuroscience & therapeutics · 2025
    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

9 authors.

Maria E BernisNeonatologie und Pädiatrische Intensivmedizin, Eltern-Kind-Zentrum, Universitätsklinikum Bonn, 53127 Bonn, Germany.
Charlotte HakvoortNeonatologie und Pädiatrische Intensivmedizin, Eltern-Kind-Zentrum, Universitätsklinikum Bonn, 53127 Bonn, Germany.
Efe NacarkucukNeonatologie und Pädiatrische Intensivmedizin, Eltern-Kind-Zentrum, Universitätsklinikum Bonn, 53127 Bonn, Germany.ORCID 0009-0005-1605-4868
Hannah BurkardNeonatologie und Pädiatrische Intensivmedizin, Eltern-Kind-Zentrum, Universitätsklinikum Bonn, 53127 Bonn, Germany.
Anna-Sophie BremerNeonatologie und Pädiatrische Intensivmedizin, Eltern-Kind-Zentrum, Universitätsklinikum Bonn, 53127 Bonn, Germany.
Margit ZweyerNeonatologie und Pädiatrische Intensivmedizin, Eltern-Kind-Zentrum, Universitätsklinikum Bonn, 53127 Bonn, Germany.ORCID 0000-0001-5615-1869
Elke MaesNeonatologie und Pädiatrische Intensivmedizin, Eltern-Kind-Zentrum, Universitätsklinikum Bonn, 53127 Bonn, Germany.
Kora A GrzelakNeonatologie und Pädiatrische Intensivmedizin, Eltern-Kind-Zentrum, Universitätsklinikum Bonn, 53127 Bonn, Germany.
Hemmen SabirNeonatologie und Pädiatrische Intensivmedizin, Eltern-Kind-Zentrum, Universitätsklinikum Bonn, 53127 Bonn, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neonatal hypoxic-ischemic encephalopathy is the most common cause of long-term disability in term neonates, and white matter injury is the primary cause of cerebral palsy. Therapies that focus on the neuroprotection of myelination and oligodendrocyte proliferation could potentially ameliorate long-lasting neurological impairments after hypoxic-ischemic encephalopathy. Clemastine, a histamine H1 antagonist, has been shown to exert neuroprotective effects in multiple sclerosis and spinal cord injury by promoting oligodendrogenesis and re-myelination. In this study, we demonstrated the neuroprotective effects of clemastine in our rat model of neonatal hypoxic-ischemic brain injury. Animals received a single intraperitoneal injection of either vehicle or clemastine (10 mg/kg) for 6 consecutive days. Our results showed a significant reduction in white matter loss after treatment, with a clear effect of clemastine on oligodendrocytes, showing a significant increase in the number of Olig2+ cells. We characterized the MAPK/ERK pathway as a potential mechanistic pathway underlying the neuroprotective effects of clemastine. Altogether, our results demonstrate that clemastine is a potential compound for the treatment of hypoxic-ischemic encephalopathy, with a clear neuroprotective effect on white matter injury by promoting oligodendrogenesis.

Indexed as

Animals, NewbornCell ProliferationClemastineDisease Models, AnimalHypoxia-Ischemia, BrainMAP Kinase Signaling SystemNeuroprotective AgentsOligodendrogliaAnimalsRatsRats, Sprague-DawleyClemastineNeuroprotective Agentsclemastinehypoxiainjuryischemianeuroprotectiveoligodendrogenesiswhite matter

Identifiers

PMID39125778
PMCPMC11311837

What Socratic holds

Textmetadata
LicenceCC BY
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.