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Molecular Mechanisms and Signaling Pathways in Neurodegenerative Disorders
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Molecular Mechanisms and Signaling Pathways in Neurodegenerative Disorders

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: 31 May 2024 | Viewed by 1460

Special Issue Editor

Dr. Andrea Kwakowsky

E-Mail Website
Guest Editor
Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
Interests: neuroscience; Alzheimer's and Huntington's disease; human neurodegenerative diseases; gamma-aminobutyric acid (GABA) and glutamate signalling; estrogen signalling; neurotrophin signalling; neuroprotection; neuroinflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue of IJMS provides a forum for the dissemination of the most recent findings on molecular mechanisms and signaling pathways involved in neurodegenerative diseases.

Neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, Amyotrophic Lateral Sclerosis and Multiple Sclerosis pose extraordinary challenges for research and society. There is a pressing need for therapies to prevent and/or slow the progression of these disorders.

While several factors are thought to contribute to the neurodegenerative process, such as oxidative stress, excitotoxicity, protein aggregation, vascular dysfunction and neuroinflammation, understanding the disease pathology and mechanisms involved are key in identifying potential therapeutic targets. In order to design effective therapies, it is fundamental to conduct studies aimed at increasing understanding of the underlying pathology.

We welcome the submission of original research and review articles on the advances in every aspect of research of molecular mechanisms and signaling pathways relevant to neurodegenerative diseases.

Dr. Andrea Kwakowsky
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

  • Alzheimer's and Huntington's disease
  • human neurodegenerative diseases
  • gamma-aminobutyric acid (GABA) and glutamate signalling
  • estrogen signalling
  • neurotrophin signalling

Published Papers (1 paper)

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Research

17 pages, 11548 KiB  
Article
Tonabersat Significantly Reduces Disease Progression in an Experimental Mouse Model of Multiple Sclerosis
by Andrea Kwakowsky, Bhavya Chawdhary, Antonio de Souza, Emily Meyer, Andrew H. Kaye, Colin R. Green, Stanley S. Stylli and Helen Danesh-Meyer
Int. J. Mol. Sci. 2023, 24(24), 17454; https://doi.org/10.3390/ijms242417454 - 14 Dec 2023
Cited by 1 | Viewed by 1057
Abstract
Multiple sclerosis (MS) is a neurodegenerative disease marked by chronic neuroinflammation thought to be mediated by the inflammasome pathway. Connexin 43 (Cx43) hemichannels contribute to the activation of the inflammasome through the release of adenosine triphosphate (ATP) inflammasome activation signals. The objective of [...] Read more.
Multiple sclerosis (MS) is a neurodegenerative disease marked by chronic neuroinflammation thought to be mediated by the inflammasome pathway. Connexin 43 (Cx43) hemichannels contribute to the activation of the inflammasome through the release of adenosine triphosphate (ATP) inflammasome activation signals. The objective of the study was to evaluate if the Cx43 hemichannel blocker, tonabersat, is effective in modulating the inflammatory response and reducing disability in the myelin oligodendrocyte glycoprotein 35–55-induced experimental autoimmune encephalomyelitis (MOG35–55 EAE) model of MS. Here, we show that the Cx43 hemichannel blocking drug, tonabersat, significantly reduced expression of neuroinflammatory markers for microglial activation (ionized calcium-binding adapter molecule 1 (Iba1)) and astrogliosis (glial fibrillary acidic protein (GFAP)) while preserving myelin basic protein (MBP) expression levels in the corpus callosum, motor cortex, and striatum regions of the brain in MOG35–55 EAE mice. Reduced NOD-like receptor protein 3 (NLRP3) inflammasome complex assembly and Caspase-1 activation confirmed the drug’s mode of action. MOG35–55 EAE mice showed clinical signs of MS, but MOG35–55 EAE mice treated with tonabersat retained behavior closer to normal. These data suggest that clinical trial phase IIb-ready tonabersat may merit further investigation as a promising candidate for MS treatment. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Signaling Pathways in Neurodegenerative Disorders)
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