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Molecular Research in Epilepsy and Epileptogenesis—2nd Edition
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Molecular Research in Epilepsy and Epileptogenesis—2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 January 2026 | Viewed by 1209

Special Issue Editor

Prof. Dr. Stanisław Jerzy Czuczwar

E-Mail Website
Guest Editor
Department of Pathophysiology, Medical University of Lublin, 20-090 Lublin, Poland
Interests: Alzheimer; epilepsy; stroke
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleauges,

Epilepsy is a neurological disorder affecting approximately 65 million people worldwide. In about 30% of patients with epilepsy, seizures are poorly controlled with antiseizure (antiepileptic) drugs, and drug-resistant epilepsy poses a significant therapeutic problem. Thus, there is a need for more efficient treatments of epilepsy in order to obtain freedom from seizures in a more significant proportion of patients. The molecular targets for available antiseizure drugs have been recognized, and the identification of novel targets and their ligands should result in the development of innovative drugs sharing additional mechanisms of action.

Antiseizure drugs are generally not effective against epileptogenesis that is triggered by an initial insult  (e.g., status epilepticus, head trauma or stroke). The durable process of epileptogenesis has been proven to convert a normally functioning mammalian brain into one generating seizure activity. A possibility arises that stopping or slowing down the progress of epileptogenesis may prevent the occurrence of epilepsy. Certainly, anti-epileptogenic drugs would be most effective prior to seizure activity, so markers for epileptogenesis are required.

Considering what was stated above, this Special Issue on "Molecular Research in Epilepsy and Epileptogenesis—2nd Edition" is open to research dealing with molecular mechanisms of seizure activity or epileptogenesis and focused on possible targets for antiseizure and anti-epileptogenic drugs. Original and review papers based on in vitro experiments, animal models of seizures also aimed at the process of epileptogenesis, and clinical studies are invited

Prof. Dr. Stanisław Jerzy Czuczwar
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • epilepsy
  • antiseizure
  • anti-epileptogenic drugs
  • biomarkers

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Published Papers (2 papers)

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21 pages, 3323 KiB  
Article
Subcortical Circuits Among Pedunculopontine Nucleus, Thalamus and Basal Ganglia Play Important Roles in Paroxysmal Arousal in Genetic Rat Models of Autosomal Dominant Sleep-Related Hypermotor Epilepsy
by Ruri Okubo, Eishi Motomura and Motohiro Okada
Int. J. Mol. Sci. 2025, 26(12), 5522; https://doi.org/10.3390/ijms26125522 - 9 Jun 2025
Viewed by 306
Abstract
A part of autosomal dominant sleep-related hypermotor epilepsy (ADSHE) is caused by mutant CHRNA4. The pathomechanisms underlying motor seizures followingly brief/sudden awakening (paroxysmal arousal) in ADSHE seizures remain to be clarified. This study determined extracellular levels of ACh and L-glutamate in the pedunculopontine [...] Read more.
A part of autosomal dominant sleep-related hypermotor epilepsy (ADSHE) is caused by mutant CHRNA4. The pathomechanisms underlying motor seizures followingly brief/sudden awakening (paroxysmal arousal) in ADSHE seizures remain to be clarified. This study determined extracellular levels of ACh and L-glutamate in the pedunculopontine nucleus (PPN) and its projection regions, including the thalamus and basal ganglia, during wakefulness, slow-wave sleep (SWS) and paroxysmal arousal of transgenic rats bearing rat S286L-mutant Chrna4 (S286L-TG), corresponding to human S284L-mutant CHRNA4, using microdialysis. The expression of connexin43 and pannexin1 in the plasma membrane of the PPN was determined using capillary immunoblotting. The expressions of connexin43 and pannexin1 in the PPN plasma membrane of S286L-TG were larger than the wild type. The extracellular L-glutamate levels in the PPN and projection regions of S286L-TG consistently increased during both wakefulness and SWS compared to the wild type. The extracellular levels of ACh and L-glutamate in the PPN and projection regions decreased accompaning SWS in the wild type. In S286L-TG, this decreasing extracellular ACh level was observed, whereas decreasing L-glutamate level was impaired. Both extracellular levels of ACh and L-glutamate in the PPN and projection regions drastically increased during paroxysmal arousal. Hemichannel inhibitors suppressed the increasing releases of ACh and L-glutamate induced by paroxysmal arousal but decreased and did not affect extracellular levels of L-glutamate and ACh during wakefulness and SWS, respectively. In particular, under hemichannels inhibition, decreasing L-glutamate release accompanying SWS was observed in S286L-TG. This study elucidated that enhanced hemichannels are predominantly involved in the dysfunction of glutamatergic transmission compared to AChergic transmission during the interictal stage in S286L-TG, whereas the hyperactivation of hemichannels contributes to the generation of paroxysmal arousal. Therefore, the hyperactivated excitatory tripartite synaptic transmission associated with hemichannels in the PPN and projection regions plays important roles in epileptogenesis/ictogenesis in S286L-TG. Full article
(This article belongs to the Special Issue Molecular Research in Epilepsy and Epileptogenesis—2nd Edition)
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14 pages, 1614 KiB  
Article
Identification of Plasma Growth Factors and Cytokines as Diagnostic Biomarkers for the Lafora Form of Progressive Myoclonus Epilepsy
by Mireia Moreno-Estellés, María Machio, Laura González, Marta Albuixech, Laura Abraira, Manuel Quintana, Manuel Toledo, Marina P. Sánchez, José M. Serratosa and Pascual Sanz
Int. J. Mol. Sci. 2025, 26(11), 5354; https://doi.org/10.3390/ijms26115354 - 3 Jun 2025
Viewed by 712
Abstract
Lafora progressive myoclonus epilepsy (LD, OMIM#254780, ORPHA:501) is an ultra-rare and severe autosomal recessive neurological disorder that typically manifests in early adolescence. It is characterized by the accumulation of insoluble forms of aberrant glycogen in the brain and peripheral tissues. Given the urgent [...] Read more.
Lafora progressive myoclonus epilepsy (LD, OMIM#254780, ORPHA:501) is an ultra-rare and severe autosomal recessive neurological disorder that typically manifests in early adolescence. It is characterized by the accumulation of insoluble forms of aberrant glycogen in the brain and peripheral tissues. Given the urgent need for reliable tools to monitor disease progression, we aimed to identify reliable biomarkers in minimally invasive fluids, which could also provide valuable insights into the natural history of the disease. Plasma-EDTA samples from eleven LD patients and healthy controls were analyzed to identify potential biomarkers of LD using a high-throughput assay. The findings were subsequently validated using specific enzyme-linked immunosorbent assays (ELISAs). Eleven cytokines and growth factors were identified to be significantly reduced in LD patient samples compared to healthy controls. Among these, four mediators [platelet-derived growth factor subunit B (PDGF-BB), epidermal growth factor (EGF), brain derived growth factor (BDNF), and macrophage migration inhibitory factor (MIF)] exhibited the greatest fold change between the groups and were further validated. Given the minimally invasive nature of plasma sampling and the straightforward quantification via ELISA assays, these biomarkers hold strong promise for rapid translation to the clinic, potentially enhancing early diagnosis and longitudinal disease monitoring in LD patients. Full article
(This article belongs to the Special Issue Molecular Research in Epilepsy and Epileptogenesis—2nd Edition)
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