Special Issue "Drugs Targeting the Disease Progression, Cognitive Impairment, Anxiety and Other Co-morbidities in Epilepsy: From Bench to Bedside"

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Drug Metabolism".

Deadline for manuscript submissions: 15 December 2023 | Viewed by 1326

Special Issue Editors

Departamento de Química e Bioquímica and Instituto de Biosistemas e Ciências Integrativas, Faculdade de Ciências, Universidade de Lisboa, Campo Grande, 1749-016 Lisboa, Portugal
Interests: neuroscience pharmacology; toxicology and pharmaceutics chemistry psychology biochemistry; genetics and molecular biology arts and humanities
ICBAS-Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Rua de Jorge Viterbo Ferreira, 228, 4050-313 Porto, Portugal
Interests: adenosine; neuromodulation; neuromuscular junction; epilepsy; osteogenic differentiation; fibrosis; mesenchymal stem cells (MSCs)

Special Issue Information

Dear Colleagues,

Until now, epilepsy therapy has mainly focused on anticonvulsant drugs with negligible disease modifying properties.  Despite the increasing implication of non-canonical neurotransmitter systems in epilepsy, this knowledge has not been sufficiently translated into clinical practice to decrease epileptogenesis progression and accompanying neuropsychiatric co-morbidities. For instance, brain monoaminergic circuits are important regulators of synaptic plasticity and acute stress responses ultimately involved in epilepsy-induced anxiety and memory impairment, but only a few studies have proven that these circuits are altered in epilepsy. Likewise, central cholinergic system adaptations are also associated with epileptogenesis. Both monoaminergic and cholinergic brain circuits frequently target cortical interneurons, expressing a myriad of neuropeptide co-transmitters in distinct cortical areas including the hippocampus, the amygdala, and the prefrontal cortex, all involved in emotional control of cognition. On the other hand, brain neuropeptides released during high-frequency and repetitive discharges may also foster neuronal hyperexcitability states, thus facilitating seizures recurrence and chronic epilepsy. This Special Issue aims to receive high-quality original research papers and review articles focusing on novel drug targets to control epilepsy progression and neuropsychiatric co-morbidities from bench to bedside and bedside to bench perspectives.

Dr. Diana Cunha-Reis
Dr. Paulo Correia-de-Sá
Guest Editors

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  • epilepsy and epileptogenesis
  • aminergic neurotransmission
  • neuropeptidergic neuromodulation
  • interneurons
  • neuroprotection
  • neuroplasticity
  • cognitive impairment
  • anxiety
  • neuropsychiatric co-morbidities

Published Papers (1 paper)

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Evaluation of the Antioxidant Activity of Levetiracetam in a Temporal Lobe Epilepsy Model
Biomedicines 2023, 11(3), 848; https://doi.org/10.3390/biomedicines11030848 - 10 Mar 2023
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Epilepsy is a neurological disorder in which it has been shown that the presence of oxidative stress (OS) is implicated in epileptogenesis. The literature has shown that some antiseizure drugs (ASD) have neuroprotective properties. Levetiracetam (LEV) is a drug commonly used as an [...] Read more.
Epilepsy is a neurological disorder in which it has been shown that the presence of oxidative stress (OS) is implicated in epileptogenesis. The literature has shown that some antiseizure drugs (ASD) have neuroprotective properties. Levetiracetam (LEV) is a drug commonly used as an ASD, and in some studies, it has been found to possess antioxidant properties. Because the antioxidant effects of LEV have not been demonstrated in the chronic phase of epilepsy, the objective of this study was to evaluate, for the first time, the effects of LEV on the oxidant–antioxidant status in the hippocampus of rats with temporal lobe epilepsy (TLE). The in vitro scavenging capacity of LEV was evaluated. LEV administration in rats with TLE significantly increased superoxide dismutase (SOD) activity, increased catalase (CAT) activity, but did not change glutathione peroxidase (GPx) activity, and significantly decreased glutathione reductase (GR) activity in comparison with epileptic rats. LEV administration in rats with TLE significantly reduced hydrogen peroxide (H2O2) levels but did not change lipoperoxidation and carbonylated protein levels in comparison with epileptic rats. In addition, LEV showed in vitro scavenging activity against hydroxyl radical (HO•). LEV showed significant antioxidant effects in relation to restoring the redox balance in the hippocampus of rats with TLE. In vitro, LEV demonstrated direct antioxidant activity against HO•. Full article
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