Evidence map›Paper›PMID 41695273›Full record

ArticleFrontiers in aging neuroscience2026

The temporal and stimuli-specific effects of LPS and IFNγ on microglial activation.

Christina N Heiss, Andrew S Naylor, Ida Pesämaa, Arketa Meshi, Benjamin Céspedes-Cortés, Chiméne Lounès, Ayat Taki, Katarina Türner Stenström, Dzeneta Vizlin-Hodzic, Henrik Zetterberg and 4 more

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Article in Frontiers in aging neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
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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

14 authors.

Christina N Heiss *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Andrew S Naylor *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Ida Pesämaa *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Arketa MeshiDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Benjamin Céspedes-CortésDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Chiméne LounèsDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Ayat TakiDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Katarina Türner StenströmDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Dzeneta Vizlin-HodzicDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Verónica PalmaLaboratory of Stem Cells and Developmental Biology, Faculty of Science, University of Chile Santiago, Chile.
Gunnar BrinkmalmDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Ann BrinkmalmDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Stefanie FruhwürthDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia, the resident immune cells of the central nervous system (CNS), play a pivotal role in health and disease maintaining homeostasis and mediating neuroinflammatory responses. Their activation is a dynamic and context-dependent process characterized by diverse phenotypic states defined by transcriptomic, proteomic, and morphological characteristics. While lipopolysaccharide (LPS) is widely used as an inflammatory stimulus in microglial research, its physiological relevance remains debated. Interferon gamma (IFNγ), a key pro-inflammatory cytokine involved in immune priming, more closely mimics CNS inflammatory conditions. In this study, we systematically investigated the temporal activation profiles of human iPSC-derived microglia (hiMG) in response to LPS, IFNγ, and their combination. Transcriptomic analysis at 24 h revealed robust differential gene expression, with over 7,000 genes altered by LPS and more than 8,500 by LPS/IFNγ co-stimulation. These profiles partially overlapped with disease-associated microglia (DAM) signatures, including upregulation of

Indexed as

DAM signatureinterferon γLPSmicroglianeuroinflammation

Identifiers

PMID41695273
PMCPMC12894321

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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.