Evidence map›Paper›PMID 42011986›Full record

ArticleGlia2026

A Cross-Disease Microglial Transcriptional Program Characterizes Neurodegeneration and Highlights SPP1 as a Biomarker.

Alessandro Palma, Roberta Stefanelli, Francesco Trenta, Chiara Projetti, Greta Massa, Sonia Canterini, Maria Teresa Fiorenza

Abstract read
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. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

7 authors.

Alessandro PalmaDivision of Neuroscience, Department of Psychology, Sapienza University of Rome, Rome, Italy.ORCID 0000-0003-1300-5479
Roberta StefanelliDivision of Neuroscience, Department of Psychology, Sapienza University of Rome, Rome, Italy.
Francesco TrentaDivision of Neuroscience, Department of Psychology, Sapienza University of Rome, Rome, Italy.
Chiara ProjettiDivision of Neuroscience, Department of Psychology, Sapienza University of Rome, Rome, Italy.
Greta MassaDivision of Neuroscience, Department of Psychology, Sapienza University of Rome, Rome, Italy.
Sonia CanteriniDivision of Neuroscience, Department of Psychology, Sapienza University of Rome, Rome, Italy.
Maria Teresa FiorenzaDivision of Neuroscience, Department of Psychology, Sapienza University of Rome, Rome, Italy.

Funding

Fondazione Telethon GSP20006_Covid050Sapienza Università di Roma RG1221816B9646F5Sapienza Università di Roma RM123188F700A7B2
6 · The paper itself

Abstract

Microglial cells are key players in maintaining brain homeostasis and responding to pathological conditions. Their multifaceted roles in health and disease have garnered significant attention in the context of neurodegeneration. In recent years, single-cell transcriptomic techniques have provided unprecedented insights into microglial heterogeneity, revealing distinct subpopulations and gene expression patterns associated with neuroprotection or neurotoxicity. Here, we dissect the transcriptomic landscape of microglia by leveraging human single-nuclei RNA sequencing datasets from multiple neurodegenerative conditions, including Amyotrophic Lateral Sclerosis, frontotemporal dementia, Alzheimer's disease, aging, and Parkinson's disease. This integrative analysis identifies distinct microglial subpopulations, reflecting functional heterogeneity across diseases and reveals a shared cross-disease microglial transcriptional program associated with inflammatory and neurodegenerative processes. Using a machine learning framework, we further demonstrate that this transcriptional program enables robust discrimination between neurodegenerative and control samples. Experimental validation in primary microglia isolated from a mouse model of Niemann-Pick disease type C, also known as juvenile Alzheimer's disease, supports the conservation of key components of this program and highlights Spp1 as a biomarker of disease-associated microglia states. Overall, this study provides an improved portrait of microglia transcriptional remodeling across neurodegenerative disorders and offers a framework for identifying conserved molecular features that may inform therapeutic strategies aimed at modulating microglial activity to mitigate disease progression and foster neuroprotection.

Indexed as

MicrogliaNeurodegenerative DiseasesOsteopontinAlzheimer DiseaseAnimalsBiomarkersHumansMiceTranscriptomeBiomarkersOsteopontinSPP1 protein, humangenomicsmacrophagesmicroglianeurodegenerationNiemann‐PickSPP1

Identifiers

PMID42011986
PMCPMC13097963

What OpenQuestion holds

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Registered trials

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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.