Evidence map›Paper›PMID 39851521›Full record

ReviewCells2025

The Role of Glial Cells in the Pathophysiology of Epilepsy.

Filiz Onat, My Andersson, Nihan Çarçak

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Immune dysregulation and epileptogenesis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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  5. KArchiv der Pharmazie · 2026
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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

3 authors.

Filiz OnatDepartment of Medical Pharmacology, School of Medicine, Acibadem Mehmet Ali Aydinlar University, 34684 Istanbul, Türkiye.ORCID 0000-0003-0680-4782
My AnderssonDepartment of Experimental Medicine, Faculty of Medicine, Lund University, 221 00 Lund, Sweden.ORCID 0000-0003-3699-138X
Nihan ÇarçakInstitute of Health Sciences, Department of Neuroscience, Acibadem Mehmet Ali Aydinlar University, 34684 Istanbul, Türkiye.ORCID 0000-0001-6254-4319

Funding

European Commission Horizon Europe Programme under the call HORIZON-WIDERA-2021-ACCESS-03 101078981- GEMSTONE
6 · The paper itself

Abstract

Epilepsy is a chronic neurological disorder marked by recurrent seizures, significantly impacting individuals worldwide. Current treatments are often ineffective for a third of patients and can cause severe side effects, necessitating new therapeutic approaches. Glial cells, particularly astrocytes, microglia, and oligodendrocytes, are emerging as crucial targets in epilepsy management. Astrocytes regulate neuronal homeostasis, excitability, and synaptic plasticity, playing key roles in maintaining the blood-brain barrier (BBB) and mediating neuroinflammatory responses. Dysregulated astrocyte functions, such as reactive astrogliosis, can lead to abnormal neuronal activity and seizure generation. They release gliotransmitters, cytokines, and chemokines that may exacerbate or mitigate seizures. Microglia, the innate immune cells of the CNS, contribute to neuroinflammation, glutamate excitotoxicity, and the balance between excitatory and inhibitory neurotransmission, underscoring their dual role in seizure promotion and protection. Meanwhile, oligodendrocytes, primarily involved in myelination, also modulate axonal excitability and contribute to the neuron-glia network underlying seizure pathogenesis. Understanding the dynamic interactions of glial cells with neurons provides promising avenues for novel epilepsy therapies. Targeting these cells may lead to improved seizure control and better clinical outcomes, offering hope for patients with refractory epilepsy.

Indexed as

EpilepsyNeurogliaAnimalsAstrocytesBlood-Brain BarrierHumansNeuronsastrocyteepileptogenesisexperimental modelmicrogliaoligodendrocytepenta-partite synapseseizure

Identifiers

PMID39851521
PMCPMC11763453

What Socratic holds

Textmetadata
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.