Evidence map›Paper›PMID 41867871›Full record

ArticlebioRxiv : the preprint server for biology2026

Single-Nucleus Transcriptomics Reveals Cell Type-Specific Remodeling and Epilepsy-Associated Microglia.

Victoria Ho, Ruth Tjondropurnomo, Jennifer Nguyen, Eszter Balkó, Samantha Depew, Xing Chen, Radhika Singh, J Edward Van Veen, Bence Rácz, Peyman Golshani

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 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

5 · Who and what money

Authors and funding

10 authors.

Victoria HoDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.ORCID 0000-0003-4159-1356
Ruth TjondropurnomoDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Jennifer NguyenDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Eszter BalkóNational Laboratory of Infectious Animal Diseases, Antimicrobial Resistance, Veterinary Public Health and Food Chain Safety, University of Veterinary Medicine Budapest, Budapest, Hungary.
Samantha DepewDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Xing ChenDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Radhika SinghDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
J Edward Van VeenDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.ORCID 0000-0003-1798-3210
Bence RáczNational Laboratory of Infectious Animal Diseases, Antimicrobial Resistance, Veterinary Public Health and Food Chain Safety, University of Veterinary Medicine Budapest, Budapest, Hungary.ORCID 0000-0002-1933-5332
Peyman GolshaniDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.ORCID 0000-0002-5406-7695

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesial temporal lobe epilepsy (TLE) is the most common form of acquired epilepsy involving the hippocampus and is a frequent sequelae of head trauma. TLE is associated with refractory seizures and significant cognitive deficits. Yet, the gene expression patterns and cell types driving epileptogenesis and the associated cognitive deficits are poorly understood. To address this, we performed single nucleus RNA sequencing on hippocampal tissue from mice at 3 and 6 weeks following pilocarpine-induced status epilepticus, a robust model of TLE. At these early timepoints, epilepsy samples showed reductions in specific Cck and Lamp5-Lhx6 interneuron subclusters, alongside increases in Cajal-Retzius cells, dentate granule (DG) cell precursors, and a mature DG cell subcluster. Among glia, an astrocyte subcluster and a markedly expanded microglia sublcuster were increased. We term this microglia population epilepsy-associated microglia (EAM). The transcriptomic profile of EAM partially overlaps with microglia described in models of Alzheimer's disease and traumatic brain injury, with enrichment of genes including

Identifiers

PMID41867871
PMCPMC13001477

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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.