Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Epilepsy: Molecular Mechanisms and Therapies
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Epilepsy: Molecular Mechanisms and Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 November 2024) | Viewed by 6222

Special Issue Editors

Dr. Dorota Teresa Nieoczym

E-Mail Website
Guest Editor
Department of Animal Physiology and Pharmacology, Institute of Biological Sciences, Faculty of Biology and Biotechnology, Maria Curie-Skłodowska University, Akademicka 19, 20-033 Lublin, Poland
Interests: neuropharmacology; behavioral neuroscience; epilepsy; depression; anxiety, natural compounds
Special Issues, Collections and Topics in MDPI journals
Dr. Kinga Gawel

E-Mail Website
Guest Editor
Department of Experimental and Clinical Pharmacology, Medical University of Lublin, 8b Jaczewskiego Str., 20-090 Lublin, Poland
Interests: epilepsy; neuropharmacology; zebrafish; behavioral neuroscience; genetic models; screening; deep phenotyping
Special Issues, Collections and Topics in MDPI journals
Dr. Agnieszka Zelek-Molik

E-Mail Website
Guest Editor
Department of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343 Kraków, Poland
Interests: neurobiology; pharmacology; stress; psychiatric disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epilepsy is a severe and chronic disorder of the central nervous system that affects about 1% of the population worldwide. It is characterized by recurrent and spontaneous seizures which result from excessive electrical discharges of neurons in various parts of the brain. Seizures might manifest as short periods of unconsciousness as well as disturbances in sensory, motor, or vegetative functions, and might also prolong to status epilepticus. Although pharmacotherapy is the main treatment for epilepsy, the currently available antiseizure drugs do not cure epilepsy but only allow a reduction in the intensity and/or frequency of epileptic seizures. Moreover, anticonvulsant medication often provokes numerous side effects.

The aim of this Special Issue on “Epilepsy: Molecular Mechanisms and Therapies” is to collect innovative research focused on various aspects of the molecular mechanisms of epileptic disorders and epileptogenesis. We are also interested in papers that present some new therapy possibilities for epilepsy and comorbid diseases. Preclinical studies from in vitro tests and animal models as well as clinical studies will be considered.

We look forward to your manuscript submission in the form of original papers, reviews and short communications.

Dr. Dorota Teresa Nieoczym
Dr. Kinga Gawel
Dr. Agnieszka Zelek-Molik
Guest Editors

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

  • seizures
  • epileptogenesis
  • anticonvulsant drugs
  • ion channels
  • neurotransmitters
  • molecular mechanisms
  • epilepsy/seizure models

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Other

29 pages, 8340 KiB  
Article
In Silico Analysis, Anticonvulsant Activity, and Toxicity Evaluation of Schisandrin B in Zebrafish Larvae and Mice
by Dorota Nieoczym, Nancy Saana Banono, Katarzyna Stępnik, Agnieszka A. Kaczor, Przemysław Szybkowski, Camila Vicencio Esguerra, Wirginia Kukula-Koch and Kinga Gawel
Int. J. Mol. Sci. 2023, 24(16), 12949; https://doi.org/10.3390/ijms241612949 - 18 Aug 2023
Cited by 2 | Viewed by 2072
Abstract
The aim of this study is to evaluate the anticonvulsant potential of schisandrin B, a main ingredient of Schisandra chinensis extracts. Schisandrin B showed anticonvulsant activity in the zebrafish larva pentylenetetrazole acute seizure assay but did not alter seizure thresholds in the intravenous [...] Read more.
The aim of this study is to evaluate the anticonvulsant potential of schisandrin B, a main ingredient of Schisandra chinensis extracts. Schisandrin B showed anticonvulsant activity in the zebrafish larva pentylenetetrazole acute seizure assay but did not alter seizure thresholds in the intravenous pentylenetetrazole test in mice. Schisandrin B crosses the blood–brain barrier, which we confirmed in our in silico and in vivo analyses; however, the low level of its unbound fraction in the mouse brain tissue may explain the observed lack of anticonvulsant activity. Molecular docking revealed that the anticonvulsant activity of the compound in larval zebrafish might have been due to its binding to a benzodiazepine site within the GABAA receptor and/or the inhibition of the glutamate NMDA receptor. Although schisandrin B showed a beneficial anticonvulsant effect, toxicological studies revealed that it caused serious developmental impairment in zebrafish larvae, underscoring its teratogenic properties. Further detailed studies are needed to precisely identify the properties, pharmacological effects, and safety of schisandrin B. Full article
(This article belongs to the Special Issue Epilepsy: Molecular Mechanisms and Therapies)
►▼ Show Figures

Figure 1

Other

Jump to: Research

16 pages, 1927 KiB  
Brief Report
A Novel Genetic Variant in MBD5 Associated with Severe Epilepsy and Intellectual Disability: Potential Implications on Neural Primary Cilia
by Mariana Martins, Ana Rafaela Oliveira, Solange Martins, José Pedro Vieira, Pedro Perdigão, Ana Rita Fernandes, Luís Pereira de Almeida, Paulo Jorge Palma, Diana Bela Sequeira, João Miguel Marques Santos, Frederico Duque, Guiomar Oliveira, Ana Luísa Cardoso, João Peça and Catarina Morais Seabra
Int. J. Mol. Sci. 2023, 24(16), 12603; https://doi.org/10.3390/ijms241612603 - 9 Aug 2023
Cited by 1 | Viewed by 3099
Abstract
Disruptions in the MBD5 gene have been linked with an array of clinical features such as global developmental delay, intellectual disability, autistic-like symptoms, and seizures, through unclear mechanisms. MBD5 haploinsufficiency has been associated with the disruption of primary cilium-related processes during early cortical [...] Read more.
Disruptions in the MBD5 gene have been linked with an array of clinical features such as global developmental delay, intellectual disability, autistic-like symptoms, and seizures, through unclear mechanisms. MBD5 haploinsufficiency has been associated with the disruption of primary cilium-related processes during early cortical development, and this has been reported in many neurodevelopmental disorders. In this study, we describe the clinical history of a 12-year-old child harboring a novel MBD5 rare variant and presenting psychomotor delay and seizures. To investigate the impact of MBD5 haploinsufficiency on neural primary cilia, we established a novel patient-derived cell line and used CRISPR-Cas9 technology to create an isogenic control. The patient-derived neural progenitor cells revealed a decrease in the length of primary cilia and in the total number of ciliated cells. This study paves the way to understanding the impact of MBD5 haploinsufficiency in brain development through its potential impact on neural primary cilia. Full article
(This article belongs to the Special Issue Epilepsy: Molecular Mechanisms and Therapies)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop