Evidence map›Paper›PMID 42552722›Full record

ArticleGlia2026

Predicting Relevant Microglia-Associated Cell-Cell Communication Pathways in Alzheimer's Disease: A Role for SPP1.

Janssen M Kotah, Marina Trombetta Lima, Esmée C Dragt, Asimenia Voulgaroglou, Nieske Brouwer, Inge R Holtman, Susanne M Kooistra, Bart J L Eggen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Glia, 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

8 authors.

Janssen M KotahDepartment of Biomedical Sciences, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0000-0003-3005-730X
Marina Trombetta LimaDepartment of Biomedical Sciences, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0000-0002-3687-6210
Esmée C DragtDepartment of Biomedical Sciences, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0009-0001-1321-6412
Asimenia VoulgaroglouDepartment of Biomedical Sciences, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0009-0005-4784-108X
Nieske BrouwerDepartment of Biomedical Sciences, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Inge R HoltmanDepartment of Biomedical Sciences, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0000-0001-9752-4756
Susanne M KooistraDepartment of Biomedical Sciences, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0000-0003-0211-8283
Bart J L EggenDepartment of Biomedical Sciences, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0000-0001-8941-0353

Funding

Alzheimer Nederland WE.03-2020-03Alzheimer Nederland WE.03-2025-06Stichting De Cock-HaddersZonMw MODEM 10510032120006
6 · The paper itself

Abstract

Microglia play a key role in the pathophysiology of Alzheimer's Disease (AD) and their increased heterogeneity likely affects disease progression. We previously identified distinct microglial signatures that were enriched in AD donors and associated with amyloid and tau, respectively. Here we generated a snRNAseq dataset from postmortem control and AD cases and analyzed alterations in cell-cell communication pathways that might be relevant to AD pathophysiology. One signaling pathway perturbed in AD cases involved SPP1, and while this pathway was also present in control samples, microglia-microglia SPP1 signaling was restricted to AD donors. Further analyses within microglia-microglia signaling predict AD-specific induction of GAS6-AXL signaling (from inflammatory and ribosomal microglia), and SPP1-ITGAV/ITGB5 signaling (from disease-associated and inflammatory microglia, among others). Together, these findings might in part explain the increased microglia phagocytic profile described in AD. RNAscope confirmed enrichment of SPP1 expressing microglia near amyloid plaques in AD brain tissue samples. These data indicate altered cellular communications between microglia in the AD brain.

Indexed as

Alzheimer DiseaseBrainCell CommunicationMicrogliaOsteopontinAgedAged, 80 and overFemaleHumansMalePlaque, AmyloidSignal TransductionOsteopontinAlzheimer's diseasecell–cell communicationmicrogliasingle nucleus RNA sequencingSPP1

Identifiers

PMID42552722
PMCPMC13438122

What Socratic holds

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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.