ArticleBrain and behavior2025
Botulinum Toxin Type A as a Therapeutic Agent in Epilepsy: Attenuation of Neuronal Ferroptosis and Cognitive Dysfunction.
Article in Brain and behavior, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Botulinum Toxin Type A as a Therapeutic Agent in Epilepsy: Attenuation of Neuronal Ferroptosis and Cognitive Dysfunction.Brain and behavior · 2025Article
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6 authors.
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Abstract
purposeEpilepsy is one of the most common neurological disorders with no effective drugs to prevent seizures or their progression. Iron modulation is a potential advanced treatment for seizures. We aim to investigate whether botulinum toxin type A (BoNT/A) can attenuate epilepsy-induced neuronal death and maintain cognitive function by inhibiting ferroptosis.
methodWe established an epileptic rat model and intervened with BoNT/A to assess its influence on cognitive functions and the pathological damage of hippocampal tissues. Rat hippocampal neuronal cells were treated with magnesium-free induction solution to establish an epileptic cell model and intervened using BoNT/A. Changes in ferrous ions (Fe FINDING: We found that BoNT/A attenuated epileptiform behavior and cognitive deficits and ameliorated hippocampal tissue damage in rats under lithium chloride-pilocarpine-induced epilepsy. In vitro BoNT/A treatment exerted potent neuroprotective effects on hippocampal neuronal cells treated by magnesium-free induction solution. These protective effects were related to the regulation of ferroptosis mediated by the GPX4/ACSL4/SLC7A11 proteins.
conclusionThese results suggest that BoNT/A is effective in preventing epileptic neuronal iron death and attenuates cognitive dysfunction through the ferroptosis pathway.
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