Evidence map›Paper›PMID 42120390›Full record

ArticleNature communications2026

Gpnmb defines a phagocytic state of microglia linked to cell death in prion disease mouse model.

Davide Caredio, Giovanni Mariutti, Lisa Polzer, Beatrice Gatta, Martina Cerisoli, Yasmine Laimeche, Giulia Miracca, Jeanne Droux, Mohamad El Amki, Marc Emmenegger and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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

17 authors.

Davide Caredio *Institute of Neuropathology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0002-3723-894X
Giovanni Mariutti *Institute of Neuropathology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.
Lisa PolzerInstitute of Neuropathology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.ORCID http://orcid.org/0009-0007-5279-0883
Beatrice GattaDepartment of Quantitative Biomedicine, University of Zurich, Zurich, Switzerland.
Martina CerisoliInstitute of Neuropathology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.
Yasmine LaimecheInstitute of Neuropathology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.
Giulia MiraccaInstitute of Neuropathology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.
Jeanne DrouxDepartment of Neurology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.
Mohamad El AmkiDepartment of Neurology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0003-1245-5283
Marc EmmeneggerInstitute of Neuropathology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.
Marian Hruska-PlochanDepartment of Quantitative Biomedicine, University of Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0002-9253-4362
Susanne WegenerDepartment of Neurology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0003-4369-7023
Magdalini PolymenidouDepartment of Quantitative Biomedicine, University of Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0003-1271-9445
Matthias SchmitzDepartment of Neurology, National Reference Center for TSE, Georg-August University, Göttingen, Germany.
Inga ZerrDepartment of Neurology, National Reference Center for TSE, Georg-August University, Göttingen, Germany.
Elena De CeccoInstitute of Neuropathology, University Hospital Zurich, University of Zurich, Zurich, Switzerland. elena.dececco@uzh.ch.ORCID http://orcid.org/0000-0002-0148-2596
Adriano AguzziInstitute for the Science of the Aging Brain (ISAB), St. Gallen, Switzerland. adriano.aguzzi@isab.science.ORCID http://orcid.org/0000-0002-0344-6708

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative disorders display brain region tropism accompanied by the emergence of distinct cellular states that contribute to disease pathogenesis, with molecular alterations occurring predominantly in glial cells. Here we show the emergence of a microglial state with distinct spatial distribution in the brains of terminally sick prion-infected mice characterized by high expression of Gpnmb (glycoprotein non-metastatic melanoma protein B), transcriptional signatures consistent with phagocytic activity, and increased expression of lysosomal genes in regions undergoing pronounced cell death. We find that this cellular state is not induced by pathological protein aggregates but by soluble factors released by dying cells regardless of the initiating insult. This work defines Gpnmb⁺ microglia as a distinct phagocytic state that links cell death to microglial activation and reveals a generalizable mechanism by which microglia respond to cell loss.

Indexed as

Eye ProteinsMembrane GlycoproteinsMicrogliaPhagocytosisPrion DiseasesAnimalsBrainCell DeathDisease Models, AnimalLysosomesMiceMice, Inbred C57BLEye ProteinsGpnmb protein, mouseMembrane Glycoproteins

Identifiers

PMID42120390
PMCPMC13365222

What OpenQuestion 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 OpenQuestion graph.