ArticleGlia2026
Deletion of Astrocytic TNFR1 Attenuates Hyperexcitability and Initiation of Epileptogenesis.
Article in Glia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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7 authors.
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Abstract
Temporal lobe epilepsy (TLE), the most common form of adult focal epilepsy, is highly resistant to current medical therapy. Cytokine signaling, including via tumor necrosis factor-alpha (TNFα), has been implicated not only as an accompanying factor but as a key aspect in the initiation of the disease. TNFα, through its type-1 receptor (TNFR1) in astrocytes, controls excitatory circuits in the hippocampus, yet it remains unknown whether this astrocyte pathway specifically contributes to epilepsy. Here, we used a conditional cell-specific knockout mouse line to induce TNFR1 deletion selectively in astrocytes and test its roles in the initiation and progression of TLE. Mice lacking astrocyte TNFR1 showed decreased basal spectral power, longer latency to first seizure following treatment with kainic acid, and a less severe phenotype up to 4 weeks later. Thus, abrogation of astrocyte TNFR1 signaling may be beneficial in TLE and could provide a new therapeutic target for this disease.
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