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Updated: Aug 26, 2026

Electrophoretic Delivery of γ-aminobutyric Acid (GABA) into Epileptic Focus Prevents Seizures in Mice
Published on: May 16, 2019
Neuroprotection and epilepsy
1National Institute of Psychiatry and Neurology, Epilepsy centre, Budapest, Huvösvölgyi út 116. H-1021 Hungary.
Abstract:
During the last years it has become obvious that the current way of treating epilepsy with antiepeileptic drugs is insufficient concerning the modification of the underlying disesease and provides merely a symptomatic treatment, without clear influence on the course of the disease. There is a pressing need to find alternative strategies and to find possibilities to intervene either into the basic processes determining the development of epilepsies or to promote compensatory processes in repairing these dysfunctions. The increasing knowledge about the basic neuronal changes underlying epilepsies allows now to analyse the potential role of neuroprotective agents in in epileptogenesis. In epilepsy the most frequent constellation is the presence of damage and overexcitation together. Increase in excitability may develop after a primary damage as in posttraumatic epilepsy, or outburst of epileptic excitability may cause neuronal damage as in cell loss after status epilepticus or in any case of the so called cytotoxic damage from extensive glutamatergic involvement. Epilepsy in certain forms is a progressive disease. The factors determining the progressive course and the possibe prevention of it is obviously an overlaping field with neuroprotection. Therefore although neuroprotection works only against certain aspects of a complex cascade of pathological events, might be a promising option in several stadiums during the development and course of epilepsy. We provide evidences that some of the new antiepileptic drugs have neuroprotective effect on different animal models of chronic partial epilepsies, and how this effect is fitting to the antiepileptogenic, and seizure supressing effect of the same drugs.
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