Evidence map›Paper›PMID 38254312›Full record

ArticleBrain pathology (Zurich, Switzerland)2024

The relation between BTK expression and iron accumulation of myeloid cells in multiple sclerosis.

Anja Steinmaurer, Christian Riedl, Theresa König, Giulia Testa, Ulrike Köck, Jan Bauer, Hans Lassmann, Romana Höftberger, Thomas Berger, Isabella Wimmer and 1 more

Open access · goldAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

15 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Bruton Tyrosine Kinase in Lesions of Multiple Sclerosis and 3 of Its Models.Neurology(R) neuroimmunology & neuroinflammation · 2025
    Article
  5. Beyond relapses: How BTK inhibitors are shaping the future of progressive MS treatment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
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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

11 authors at 1 institution in 1 country.

Anja SteinmaurerDepartment of Neurology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-2389-1892
Christian RiedlDivision of Neurochemistry and Neuropathology, Medical University of Vienna, Vienna, Austria.
Theresa KönigDepartment of Neurology, Medical University of Vienna, Vienna, Austria.
Giulia TestaDivision of Neurochemistry and Neuropathology, Medical University of Vienna, Vienna, Austria.
Ulrike KöckDepartment of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.
Jan BauerDepartment of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.
Hans LassmannDepartment of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.ORCID 0000-0001-8617-5052
Romana HöftbergerDivision of Neurochemistry and Neuropathology, Medical University of Vienna, Vienna, Austria.
Thomas BergerDepartment of Neurology, Medical University of Vienna, Vienna, Austria.
Isabella WimmerDepartment of Neurology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-2231-2120
Simon HametnerDivision of Neurochemistry and Neuropathology, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · AT

Funding

Merck Healthcare KGaA
6 · The paper itself

Abstract

Activation of Bruton's tyrosine kinase (BTK) has been shown to play a crucial role in the proinflammatory response of B cells and myeloid cells upon engagement with B cell, Fc, Toll-like receptor, and distinct chemokine receptors. Previous reports suggest BTK actively contributes to the pathogenesis of multiple sclerosis (MS). The BTK inhibitor Evobrutinib has been shown to reduce the numbers of gadolinium-enhancing lesions and relapses in relapsing-remitting MS patients. In vitro, BTK inhibition resulted in reduced phagocytic activity and modulated BTK-dependent inflammatory signaling of microglia and macrophages. Here, we investigated the protein expression of BTK and CD68 as well as iron accumulation in postmortem control (n = 10) and MS (n = 23) brain tissue, focusing on microglia and macrophages. MS cases encompassed active, chronic active, and inactive lesions. BTK

Indexed as

Agammaglobulinaemia Tyrosine KinaseIronMultiple SclerosisAdultAgedAntigens, CDAntigens, Differentiation, MyelomonocyticBrainFemaleHumansMacrophagesMaleMicrogliaMiddle AgedMyeloid CellsPiperidinesAgammaglobulinaemia Tyrosine KinaseAntigens, CDAntigens, Differentiation, MyelomonocyticBTK protein, humanevobrutinibIronPiperidinesPyrimidinesBruton's tyrosine kinaseEvobrutinibmicrogliamultiple sclerosismyeloid cellsneuroinflammation

Identifiers

PMID38254312
PMCPMC11328345
OpenAlexW4391143640

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.