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Cells
Special Issues
New Strategies in Therapeutic Targets of Epilepsy
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New Strategies in Therapeutic Targets of Epilepsy

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 August 2024) | Viewed by 4460

Special Issue Editor

Dr. Cameron S. Metcalf

E-Mail Website
Guest Editor
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT 84112, USA
Interests: drug development; sudden unexpected death in epilepsy; Dravet syndrome

Special Issue Information

Dear Colleagues,

We have been fortunate to see new drugs with diverse mechanisms of action enter into clinical use for epilepsy in recent years. However, as many of us are aware, we have not been able to reduce the proportion of individuals with epilepsy whose seizures are not fully controlled. Nevertheless, exciting ongoing efforts continue to identify and validate novel targets and therapeutic approaches. This Special Issue will be focused on new strategies for identifying and validating therapeutic targets for epilepsy. This will include, but is not limited to, (1) novel mechanisms for the treatment of epilepsy and its comorbidities; (2) novel tools and approaches in target identification/validation, drug screening/differentiation, tolerability assessment and de-risking of potential therapies; and (3) novel targets and/or approaches for disease-modifying or anti-epileptogenic therapies. Articles within these general areas may be focused on unique populations (e.g., rare epilepsies) or may be applicable to a wider range of epilepsy disorders. 

We hope that you will consider submitting to this Special Issue.

Dr. Cameron S. Metcalf
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • drug development
  • animal models
  • epilepsy
  • seizure
  • rare epilepsy
  • traumatic brain injury
  • epileptogenesis
  • disease modification
  • drug discovery

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Published Papers (2 papers)

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16 pages, 2881 KiB  
Article
Cannabidiol Exerts Anticonvulsant Effects Alone and in Combination with Δ9-THC through the 5-HT1A Receptor in the Neocortex of Mice
by Yasaman Javadzadeh, Alexandra Santos, Mark S. Aquilino, Shanthini Mylvaganam, Karolina Urban and Peter L. Carlen
Cells 2024, 13(6), 466; https://doi.org/10.3390/cells13060466 - 7 Mar 2024
Cited by 1 | Viewed by 2710
Abstract
Cannabinoids have shown potential in drug-resistant epilepsy treatment; however, we lack knowledge on which cannabinoid(s) to use, dosing, and their pharmacological targets. This study investigated (i) the anticonvulsant effect of Cannabidiol (CBD) alone and (ii) in combination with Delta-9 Tetrahydrocannabinol (Δ9-THC), [...] Read more.
Cannabinoids have shown potential in drug-resistant epilepsy treatment; however, we lack knowledge on which cannabinoid(s) to use, dosing, and their pharmacological targets. This study investigated (i) the anticonvulsant effect of Cannabidiol (CBD) alone and (ii) in combination with Delta-9 Tetrahydrocannabinol (Δ9-THC), as well as (iii) the serotonin (5-HT)1A receptor’s role in CBD’s mechanism of action. Seizure activity, induced by 4-aminopyridine, was measured by extracellular field recordings in cortex layer 2/3 of mouse brain slices. The anticonvulsant effect of 10, 30, and 100 µM CBD alone and combined with Δ9-THC was evaluated. To examine CBD’s mechanism of action, slices were pre-treated with a 5-HT1A receptor antagonist before CBD’s effect was evaluated. An amount of ≥30 µM CBD alone exerted significant anticonvulsant effects while 10 µM CBD did not. However, 10 µM CBD combined with low-dose Δ9-THC (20:3 ratio) displayed significantly greater anticonvulsant effects than either phytocannabinoid alone. Furthermore, blocking 5-HT1A receptors before CBD application significantly abolished CBD’s effects. Thus, our results demonstrate the efficacy of low-dose CBD and Δ9-THC combined and that CBD exerts its effects, at least in part, through 5-HT1A receptors. These results could address drug-resistance while providing insight into CBD’s mechanism of action, laying the groundwork for further testing of cannabinoids as anticonvulsants. Full article
(This article belongs to the Special Issue New Strategies in Therapeutic Targets of Epilepsy)
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10 pages, 555 KiB  
Perspective
The Role of Glutamate and Blood–Brain Barrier Disruption as a Mechanistic Link between Epilepsy and Depression
by Benjamin F. Gruenbaum, Antonia Schonwald, Matthew Boyko and Alexander Zlotnik
Cells 2024, 13(14), 1228; https://doi.org/10.3390/cells13141228 - 21 Jul 2024
Viewed by 1390
Abstract
Epilepsy is associated with substantial neuropsychiatric impairments that persist long after the onset of the condition, significantly impacting quality of life. The goal of this review was to uncover how the pathological consequences of epilepsy, such as excessive glutamate release and a disrupted [...] Read more.
Epilepsy is associated with substantial neuropsychiatric impairments that persist long after the onset of the condition, significantly impacting quality of life. The goal of this review was to uncover how the pathological consequences of epilepsy, such as excessive glutamate release and a disrupted blood–brain barrier (BBB), contribute to the emergence of neuropsychiatric disorders. We hypothesize that epilepsy induces a dysfunctional BBB through hyperexcitation, which then further amplifies post-ictal glutamate levels and, thus, triggers neurodegenerative and neuropsychiatric processes. This review identifies the determinants of glutamate concentration levels in the brain and explores potential therapeutic interventions that restore BBB integrity. Our focus on therapeutic BBB restoration is guided by the premise that it may improve glutamate regulation, consequently mitigating the neurotoxicity that contributes to the onset of neuropsychiatric symptoms. Full article
(This article belongs to the Special Issue New Strategies in Therapeutic Targets of Epilepsy)
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