Evidence mapPaperPMID 36810097Full record

ArticleMolecular neurodegeneration2023

The Alzheimer's disease-linked protease BACE1 modulates neuronal IL-6 signaling through shedding of the receptor gp130.

Stephan A Müller, Merav D Shmueli, Xiao Feng, Johanna Tüshaus, Neele Schumacher, Ryan Clark, Brad E Smith, An Chi, Stefan Rose-John, Matthew E Kennedy and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
7.2field-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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  6. The Ubiquitin-Proteasome System in Brain Disorders: Pathogenic Pathways, Post-Translational Tweaks, and Therapeutic Frontiers.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
  7. Article
  8. Article
  9. Discovery of an APP-selective BACE1 inhibitor for Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Roles of Cytokines in Alzheimer's Disease.International journal of molecular sciences · 2024
    Review
  18. Review
  19. Article
  20. Review
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 4 institutions in 2 countries.

Stephan A Müller *German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Merav D Shmueli *German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Xiao Feng *German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Johanna TüshausGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Neele SchumacherBiochemical Institute, Kiel University, Kiel, Germany.
Ryan ClarkNeuroscience, Merck & Co. Inc., Boston, MA, USA.
Brad E SmithLaboratory Animal Resources, Merck & Co. Inc., West Point, PA, USA.
An ChiChemical Biology, Merck & Co. Inc., Boston, MA, USA.
Stefan Rose-JohnBiochemical Institute, Kiel University, Kiel, Germany.
Matthew E KennedyNeuroscience, Merck & Co. Inc., Boston, MA, USA.
Stefan F LichtenthalerGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany. stefan.lichtenthaler@dzne.de.ORCID 0000-0003-2211-2575
German Center for Neurodegenerative Diseases · DEMerck & Co., Inc., Rahway, NJ, USA (United States) · USChristian-Albrechts-Universität zu Kiel · DEUnited States Military Academy · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe protease BACE1 is a major drug target for Alzheimer's disease, but chronic BACE1 inhibition is associated with non-progressive cognitive worsening that may be caused by modulation of unknown physiological BACE1 substrates.

methodsTo identify in vivo-relevant BACE1 substrates, we applied pharmacoproteomics to non-human-primate cerebrospinal fluid (CSF) after acute treatment with BACE inhibitors.

resultsBesides SEZ6, the strongest, dose-dependent reduction was observed for the pro-inflammatory cytokine receptor gp130/IL6ST, which we establish as an in vivo BACE1 substrate. Gp130 was also reduced in human CSF from a clinical trial with a BACE inhibitor and in plasma of BACE1-deficient mice. Mechanistically, we demonstrate that BACE1 directly cleaves gp130, thereby attenuating membrane-bound gp130 and increasing soluble gp130 abundance and controlling gp130 function in neuronal IL-6 signaling and neuronal survival upon growth-factor withdrawal.

conclusionBACE1 is a new modulator of gp130 function. The BACE1-cleaved, soluble gp130 may serve as a pharmacodynamic BACE1 activity marker to reduce the occurrence of side effects of chronic BACE1 inhibition in humans.

Indexed as

Alzheimer DiseaseAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesCytokine Receptor gp130HumansInterleukin-6MiceNerve Tissue ProteinsAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBACE1 protein, humanBace1 protein, mouseCytokine Receptor gp130Interleukin-6Nerve Tissue ProteinsSez6 protein, mouseIL-6RIL-6 receptor subunit betaSecretaseSheddingTrans-signalingVCAM1

Identifiers

PMID36810097
PMCPMC9942414
OpenAlexW4321457551

What Socratic holds

Textmetadata
LicenceCC BY
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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.