Evidence map›Paper›PMID 41841337›Full record

ArticleEpilepsia2026

Long-lasting remodeling of astrocytes in an Scna1

Athénaïs Genin, Alicia Janvier, Tristan Moujellil-Legagneur, Marine Blaquière, Alexis Chaussy, Romane Privé, Fabrice Duprat, Massimo Mantegazza, Etienne Audinat, Nicola Marchi and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Epilepsia, 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. Article
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

11 authors.

Athénaïs GeninInstitute of Functional Genomics, University of Montpellier, CNRS, Inserm, Montpellier, France.ORCID https://orcid.org/0009-0004-8744-8138
Alicia JanvierInstitute of Functional Genomics, University of Montpellier, CNRS, Inserm, Montpellier, France.ORCID https://orcid.org/0009-0008-2246-4291
Tristan Moujellil-LegagneurInstitute of Functional Genomics, University of Montpellier, CNRS, Inserm, Montpellier, France.ORCID https://orcid.org/0009-0002-6842-2296
Marine BlaquièreInstitute of Functional Genomics, University of Montpellier, CNRS, Inserm, Montpellier, France.
Alexis ChaussyInstitute of Functional Genomics, University of Montpellier, CNRS, Inserm, Montpellier, France.ORCID https://orcid.org/0000-0002-3408-6303
Romane PrivéInstitute of Functional Genomics, University of Montpellier, CNRS, Inserm, Montpellier, France.ORCID https://orcid.org/0009-0004-4737-2116
Fabrice DupratUniversity Côte d'Azur, CNRS UMR7275, Inserm U1323, Institute of Molecular and Cellular Pharmacology, Valbonne-Sophia Antipolis, France.ORCID https://orcid.org/0000-0001-8774-1220
Massimo MantegazzaUniversity Côte d'Azur, CNRS UMR7275, Inserm U1323, Institute of Molecular and Cellular Pharmacology, Valbonne-Sophia Antipolis, France.ORCID https://orcid.org/0000-0002-1070-7929
Etienne AudinatInstitute of Functional Genomics, University of Montpellier, CNRS, Inserm, Montpellier, France.ORCID https://orcid.org/0000-0002-6389-422X
Nicola MarchiInstitute of Functional Genomics, University of Montpellier, CNRS, Inserm, Montpellier, France.ORCID https://orcid.org/0000-0001-9124-0226
Noémie CrestoInstitute of Functional Genomics, University of Montpellier, CNRS, Inserm, Montpellier, France.ORCID https://orcid.org/0000-0003-1029-683X

Funding

Agence Nationale de la Recherche ANR-15-IDEX-01Agence Nationale de la Recherche ANR-21-CE17-0031Agence Nationale de la Recherche ANR-22-CE14-0042Agence Nationale de la Recherche ANR-22-CE17-0061Agence Nationale de la Recherche ANR-24-CE14-3636Fondation de France
6 · The paper itself

Abstract

objectiveDravet syndrome (DS) is a prototypical developmental and epileptic encephalopathy caused by mutations in the SCN1A gene, leading to loss of function of the voltage-gated sodium channel Naᵥ1.1. The latter causes early onset drug-resistant seizures and enduring cognitive and behavioral deficits. In this pathological context, the implication of astrocytes remains insufficiently explored.

methodsUsing a heterozygous Scn1a knockout (Scn1a

resultsFrom initial disease aggravation (postnatal day [PN] 20-35) to long-term stabilization (up to PN90), Scn1a SIGNIFICANCE: In DS, astrocytes undergo long-term remodeling independent of tissue damage. We discuss the association between astrocyte network changes and seizures, as well as synaptic and cognitive deficits.

Indexed as

AstrocytesEpilepsies, MyoclonicNAV1.1 Voltage-Gated Sodium ChannelAnimalsDisease Models, AnimalElectroencephalographyGlial Fibrillary Acidic ProteinHippocampusMaleMiceMice, KnockoutGlial Fibrillary Acidic ProteinNAV1.1 Voltage-Gated Sodium ChannelScn1a protein, mouseastrocytesconnexinsdevelopmental and epileptic encephalopathyDravet syndromeneuroinflammation

Identifiers

PMID41841337
PMCPMC13285258

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.