Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Epilepsy: From Molecular Mechanisms to Targeted Therapies 3.0
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Epilepsy: From Molecular Mechanisms to Targeted Therapies 3.0

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 (30 April 2021) | Viewed by 9781

Special Issue Editor

Dr. Giuseppe Biagini

E-Mail Website
Guest Editor
Department of Biomedical, Universita degli Studi di Modena e Reggio Emilia, Modena, Italy
Interests: epilepsy; extracellular matrix; glia; hippocampus; neuroprotection; neurosteroids; seizure; stroke
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epilepsy is a neurological disorder affecting approximately 1% of the worldwide population. Despite the availability of antiepileptic drugs, one third of patients are considered “drug-resistant” and fail to achieve seizure control. In the last decade, many breakthroughs have been made in identifying different mutated genes linked to severe epilepsy, which have brought new molecular players as potential therapeutic targets. Moreover, a link between epilepsy and inflammation, which has now become an important component of the disorder, has brought several inflammatory-linked mediators as further potential therapeutic targets. To this regard, a critical role has also been suggested for blood vessels, as an altered vascularization or an abnormal response of the vessel wall during the seizure may participate in the progression of damage in the epileptic tissue. Finally, all these players could significantly modulate the process of epileptogenesis, for which a regulatory pathway such as that depending on the mammalian target of rapamycin (mTOR) is intensively studied to dissect the mechanisms leading to the development of an epileptogenic environment.

This Special Issue, “Epilepsy: From Molecular Mechanisms to Targeted Therapies”, of the International Journal of Molecular Sciences will comprise a selection of research papers and reviews covering various aspects of molecular and cellular biology of epilepsy models. Studies on bioactive molecules and nutraceutical treatments modulating epileptogenesis will also be considered.

Dr. Giuseppe Biagini
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

  • Blood-Brain Barrier
  • Epilepsy
  • Gene mutations
  • Microglia/Monocytes
  • Neuroinflammation
  • Neuroprotection

Related Special Issue

Published Papers (3 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: Review

23 pages, 3599 KiB  
Article
Src/CK2/PTEN-Mediated GluN2B and CREB Dephosphorylations Regulate the Responsiveness to AMPA Receptor Antagonists in Chronic Epilepsy Rats
by Ji-Eun Kim, Duk-Shin Lee, Hana Park and Tae-Cheon Kang
Int. J. Mol. Sci. 2020, 21(24), 9633; https://doi.org/10.3390/ijms21249633 - 17 Dec 2020
Cited by 18 | Viewed by 2309
Abstract
Both α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) and N-methyl-D-aspartate receptor (NMDAR) have been reported as targets for treatment of epilepsy. To investigate the roles and interactions of AMPAR and NMDAR in ictogenesis of epileptic hippocampus, we analyzed AMPAR antagonists (perampanel and GYKI 52466)-mediated phosphatase and [...] Read more.
Both α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) and N-methyl-D-aspartate receptor (NMDAR) have been reported as targets for treatment of epilepsy. To investigate the roles and interactions of AMPAR and NMDAR in ictogenesis of epileptic hippocampus, we analyzed AMPAR antagonists (perampanel and GYKI 52466)-mediated phosphatase and tensin homolog deleted on chromosome 10 (PTEN) regulation and glutamate ionotropic receptor NMDA type subunit 2B (GluN2B) tyrosine (Y) 1472 phosphorylation in epilepsy rats. Both perampanel and GYKI 52466 increased PTEN expression and its activity (reduced phosphorylation), concomitant with decreased activities (phosphorylations) of Src family-casein kinase 2 (CK2) signaling pathway. Compatible with these, they also restored the upregulated GluN2B Y1472 and Ca2+/cAMP response element-binding protein (CREB) serine (S) 133 phosphorylations and surface expression of glutamate ionotropic receptor AMPA type subunit 1 (GRIA1) to basal level in the epileptic hippocampus. These effects of perampanel and GYKI 52466 are observed in responders (whose seizure activities are responsive to AMPAR antagonists), but not non-responders (whose seizure activities were uncontrolled by AMPAR antagonists). Therefore, our findings suggest that Src/CK2/PTEN-mediated GluN2B Y1472 and CREB S133 regulations may be one of the responsible signaling pathways for the generation of refractory seizures in non-responders to AMPAR antagonists. Full article
(This article belongs to the Special Issue Epilepsy: From Molecular Mechanisms to Targeted Therapies 3.0)
►▼ Show Figures

Figure 1

Review

Jump to: Research

31 pages, 1526 KiB  
Review
Candidate Genes for Eyelid Myoclonia with Absences, Review of the Literature
by Sonia Mayo, Irene Gómez-Manjón, Fco. Javier Fernández-Martínez, Ana Camacho, Francisco Martínez and Julián Benito-León
Int. J. Mol. Sci. 2021, 22(11), 5609; https://doi.org/10.3390/ijms22115609 - 25 May 2021
Cited by 13 | Viewed by 2846
Abstract
Eyelid myoclonia with absences (EMA), also known as Jeavons syndrome (JS) is a childhood onset epileptic syndrome with manifestations involving a clinical triad of absence seizures with eyelid myoclonia (EM), photosensitivity (PS), and seizures or electroencephalogram (EEG) paroxysms induced by eye closure. Although [...] Read more.
Eyelid myoclonia with absences (EMA), also known as Jeavons syndrome (JS) is a childhood onset epileptic syndrome with manifestations involving a clinical triad of absence seizures with eyelid myoclonia (EM), photosensitivity (PS), and seizures or electroencephalogram (EEG) paroxysms induced by eye closure. Although a genetic contribution to this syndrome is likely and some genetic alterations have been defined in several cases, the genes responsible for have not been identified. In this review, patients diagnosed with EMA (or EMA-like phenotype) with a genetic diagnosis are summarized. Based on this, four genes could be associated to this syndrome (SYNGAP1, KIA02022/NEXMIF, RORB, and CHD2). Moreover, although there is not enough evidence yet to consider them as candidate for EMA, three more genes present also different alterations in some patients with clinical diagnosis of the disease (SLC2A1, NAA10, and KCNB1). Therefore, a possible relationship of these genes with the disease is discussed in this review. Full article
(This article belongs to the Special Issue Epilepsy: From Molecular Mechanisms to Targeted Therapies 3.0)
►▼ Show Figures

Figure 1

15 pages, 882 KiB  
Review
Links between Immune Cells from the Periphery and the Brain in the Pathogenesis of Epilepsy: A Narrative Review
by Gaku Yamanaka, Shinichiro Morichi, Tomoko Takamatsu, Yusuke Watanabe, Shinji Suzuki, Yu Ishida, Shingo Oana, Takashi Yamazaki, Fuyuko Takata and Hisashi Kawashima
Int. J. Mol. Sci. 2021, 22(9), 4395; https://doi.org/10.3390/ijms22094395 - 22 Apr 2021
Cited by 21 | Viewed by 3835
Abstract
Accumulating evidence has demonstrated that the pathogenesis of epilepsy is linked to neuroinflammation and cerebrovascular dysfunction. Peripheral immune cell invasion into the brain, along with these responses, is implicitly involved in epilepsy. This review explored the current literature on the association between the [...] Read more.
Accumulating evidence has demonstrated that the pathogenesis of epilepsy is linked to neuroinflammation and cerebrovascular dysfunction. Peripheral immune cell invasion into the brain, along with these responses, is implicitly involved in epilepsy. This review explored the current literature on the association between the peripheral and central nervous systems in the pathogenesis of epilepsy, and highlights novel research directions for therapeutic interventions targeting these reactions. Previous experimental and human studies have demonstrated the activation of the innate and adaptive immune responses in the brain. The time required for monocytes (responsible for innate immunity) and T cells (involved in acquired immunity) to invade the central nervous system after a seizure varies. Moreover, the time between the leakage associated with blood–brain barrier (BBB) failure and the infiltration of these cells varies. This suggests that cell infiltration is not merely a secondary disruptive event associated with BBB failure, but also a non-disruptive event facilitated by various mediators produced by the neurovascular unit consisting of neurons, perivascular astrocytes, microglia, pericytes, and endothelial cells. Moreover, genetic manipulation has enabled the differentiation between peripheral monocytes and resident microglia, which was previously considered difficult. Thus, the evidence suggests that peripheral monocytes may contribute to the pathogenesis of seizures. Full article
(This article belongs to the Special Issue Epilepsy: From Molecular Mechanisms to Targeted Therapies 3.0)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop