ArticleJournal of cellular and molecular medicine2026
Apoptosis and Glial Marker Profiles in Hippocampus and Amygdala of Medically Intractable Temporal Lobe Epilepsy.
Article in Journal of cellular and molecular medicine, 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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Abstract
Medically intractable temporal lobe epilepsy is associated with potential neuronal and glial damage in key brain structures, including the hippocampus and amygdala. This study aimed to examine apoptosis, caspase expression, and glial activation markers in these regions, and to evaluate their associations with clinical variables. Hippocampal and amygdala tissues from 17 patients with medically intractable epilepsy and autopsy-derived non-epileptic controls were examined for cellular apoptosis (TUNEL), caspase-3, -9, and -12, as well as GFAP (astrocytic marker) and IBA1 (microglial marker) expression using immunohistochemistry. Correlation analyses were performed to evaluate associations between these molecular markers and various clinical variables. TUNEL-positive cells and caspase-3 expression were significantly increased in both the hippocampus and amygdala of patients with medically intractable epilepsy compared to control subjects. Caspase-9 and caspase-12 were selectively elevated in the amygdala, while GFAP was upregulated in both regions, and IBA1 showed no significant differences. Protein expression patterns varied with age, sex, psychiatric comorbidities, seizure type and frequency, traumatic brain injury, and antiseizure drug treatment. Age at seizure onset, epilepsy duration, and total seizure numbers were associated with distinct molecular profiles. The epileptic hippocampal and amygdala tissues exhibit distinct, region-specific changes in apoptotic and glial markers. These findings suggest that apoptosis and glial alterations may contribute to region-specific pathological mechanisms underlying medically intractable temporal lobe epilepsy and may be influenced by clinical disease characteristics.
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