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
The Molecular Brain and Its Health
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

The Molecular Brain and Its Health

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: closed (20 September 2022) | Viewed by 5810

Special Issue Editor

Dr. Leo Veenman

E-Mail Website
Guest Editor
Consorzio per Valutazioni Biologiche e Farmacologiche, Via Nicolò Putignani, 178, 70122 Bari, Italy
Interests: drug development; brain disease and injury; mitochondrial function; genomics/non-genomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

    Studies to date indicate that the efficacious curation of brain damage, in particular neurodegeneration due to brain disease and brain injury, appears to depend on the multifaceted effects of the individual promising agents in question. To list the targets of such modulatory effects: inflammatory and/or immune response mechanisms of microglia cells; interactions between astrocytes and neurons serving to maintain the homeostatic equilibrium of the brain; oligodendritic functions serving to maintain efficient signaling from neuron to neuron; endothelial cell states underlying proper blood–brain barrier function, and even brain vascular function; programmed cell death pathways of the various cell types; regulation of stem cell activity; regeneration and wound healing.   
    This Special Issue on “The Molecular Brain and its Health” aims to gather papers addressing the abovementioned topics, in particular the underlying molecular biological mechanisms affected by the curative agents in question. Obviously, each stipulated effect in and by itself presents its own complexity. Thus, we hope that this Special Issue can bring together these singular molecular biological mechanisms. As research progresses, computational approaches also integrate the various functional pathways that will become important to conceive.

Dr. Leo Veenman
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

Drug development

Brain disease and injury

Genomics/non-genomics

Mitochondrial function

Neurons

Astrocytes

Microglia

Oligodendrocytes

Endothelial Cells

Molecular biological mechanisms

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: Review

20 pages, 2303 KiB  
Article
GABAA Receptor-Stabilizing Protein Ubqln1 Affects Hyperexcitability and Epileptogenesis after Traumatic Brain Injury and in a Model of In Vitro Epilepsy in Mice
by Tabea Kürten, Natascha Ihbe, Timo Ueberbach, Ute Distler, Malte Sielaff, Stefan Tenzer and Thomas Mittmann
Int. J. Mol. Sci. 2022, 23(7), 3902; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23073902 - 31 Mar 2022
Cited by 2 | Viewed by 2157
Abstract
Posttraumatic epilepsy (PTE) is a major public health concern and strongly contributes to human epilepsy cases worldwide. However, an effective treatment and prevention remains a matter of intense research. The present study provides new insights into the gamma aminobutyric acid A (GABAA [...] Read more.
Posttraumatic epilepsy (PTE) is a major public health concern and strongly contributes to human epilepsy cases worldwide. However, an effective treatment and prevention remains a matter of intense research. The present study provides new insights into the gamma aminobutyric acid A (GABAA)-stabilizing protein ubiquilin-1 (ubqln1) and its regulation in mouse models of traumatic brain injury (TBI) and in vitro epilepsy. We performed label-free quantification on isolated cortical GABAergic interneurons from GAD67-GFP mice that received unilateral TBI and discovered reduced expression of ubqln1 24 h post-TBI. To investigate the link between this regulation and the development of epileptiform activity, we further studied ubqln1 expression in hippocampal and cortical slices. Epileptiform events were evoked pharmacologically in acute brain slices by administration of picrotoxin (PTX, 50 μM) and kainic acid (KA, 500 nM) and recorded in the hippocampal CA1 subfield using Multi-electrode Arrays (MEA). Interestingly, quantitative Western blots revealed significant decreases in ubqln1 expression 1–7 h after seizure induction that could be restored by application of the non-selective monoamine oxidase inhibitor nialamide (NM, 10 μM). In picrotoxin-dependent dose–response relationships, NM administration alleviated the frequency and peak amplitude of seizure-like events (SLEs). These findings indicate a role of the monoamine transmitter systems and ubqln1 for cortical network activity during posttraumatic epileptogenesis. Full article
(This article belongs to the Special Issue The Molecular Brain and Its Health)
►▼ Show Figures

Figure 1

Review

Jump to: Research

12 pages, 1175 KiB  
Review
Role of Impaired Mitochondrial Dynamics Processes in the Pathogenesis of Alzheimer’s Disease
by Alexander V. Blagov, Andrey V. Grechko, Nikita G. Nikiforov, Evgeny E. Borisov, Nikolay K. Sadykhov and Alexander N. Orekhov
Int. J. Mol. Sci. 2022, 23(13), 6954; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23136954 - 23 Jun 2022
Cited by 23 | Viewed by 2610
Abstract
Mitochondrial dysfunction is now recognized as a contributing factor to neurodegenerative diseases, including Alzheimer’s disease (AD). Mitochondria are signaling organelles with a variety of functions ranging from energy production to the regulation of cellular metabolism, energy homeostasis, and response to stress. The successful [...] Read more.
Mitochondrial dysfunction is now recognized as a contributing factor to neurodegenerative diseases, including Alzheimer’s disease (AD). Mitochondria are signaling organelles with a variety of functions ranging from energy production to the regulation of cellular metabolism, energy homeostasis, and response to stress. The successful functioning of these complex processes is critically dependent on the accuracy of mitochondrial dynamics, which includes the ability of mitochondria to change shape and position in the cell, which is necessary to maintain proper function and quality control, especially in polarized cells such as neurons. There has been much evidence to suggest that the disruption of mitochondrial dynamics may play a critical role in the pathogenesis of AD. This review highlights aspects of altered mitochondrial dynamics in AD that may contribute to the etiology of this debilitating condition. We also discuss therapeutic strategies to improve mitochondrial dynamics and function that may provide an alternative treatment approach. Full article
(This article belongs to the Special Issue The Molecular Brain and Its Health)
►▼ 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