ijms-logo

Journal Browser

Journal Browser

Special Issue "CNS Drug Action in Neurodegenerative Diseases 2.0"

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: 30 September 2021.

Special Issue Editor

Prof. Dr. Stefanie Kürten
E-Mail Website
Guest Editor
Department of Neuroanatomy, Rheinische Friedrich-Wilhelms-Universität Bonn/Universitätsklinikum Bonn, Bonn, Germany
Interests: autoimmunity; autoantibodies; B cells; EAE; multiple sclerosis; neuroprotection
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Amyotrophic lateral sclerosis, multiple sclerosis, Alzheimer’s, and Parkinson’s disease are neurodegenerative diseases of the central nervous system, which represent a major socioeconomic burden to society. All of these diseases are similar in that their etiology is still unclear and there are different theories on their pathogenesis. While most drugs that are approved to treat neurodegeneration are able to reduce clinical symptoms and slow down disease progression, they cannot cure the disease. In addition, the availability of suitable biomarkers that could predict treatment success is very limited, so that patient-oriented therapy has remained a future goal. Yet, intensive research is ongoing to eventually unravel the mechanisms underlying neurodegeneration and central nervous system repair. This open-access Special Issue will bring together original research and review articles on the mode of action of different drugs that were designed to limit neurodegeneration, support neuroprotection, and/or to promote neural repair, highlighting what has already been achieved and which new discoveries, approaches, and technical developments in central nervous system research are on their way.

Topics of this Special Issue include but are not limited to:

- Etiology and pathogenesis of neurodegenerative diseases;

- Mechanisms of neurodegeneration, neuroprotection, and neural repair in the central nervous system;

- Pharmaceutical and pharmacological central nervous system drug classification;

- Mode of action of central nervous system drugs;

- Past and ongoing clinical trials using CNS drugs in neurodegenerative diseases;

- Novel strategies for the prevention and treatment of CNS degeneration.

Prof. Dr. Stefanie Kürten
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 papers will be 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

  • CNS drugs
  • neurodegenerative diseases
  • neuroprotection
  • neuroregeneration
  • pharmacology

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Open AccessArticle
Murine Esophagus Expresses Glial-Derived Central Nervous System Antigens
Int. J. Mol. Sci. 2021, 22(6), 3233; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063233 - 22 Mar 2021
Viewed by 336
Abstract
Multiple sclerosis (MS) has been considered to specifically affect the central nervous system (CNS) for a long time. As autonomic dysfunction including dysphagia can occur as accompanying phenomena in patients, the enteric nervous system has been attracting increasing attention over the past years. [...] Read more.
Multiple sclerosis (MS) has been considered to specifically affect the central nervous system (CNS) for a long time. As autonomic dysfunction including dysphagia can occur as accompanying phenomena in patients, the enteric nervous system has been attracting increasing attention over the past years. The aim of this study was to identify glial and myelin markers as potential target structures for autoimmune processes in the esophagus. RT-PCR analysis revealed glial fibrillary acidic protein (GFAP), proteolipid protein (PLP), and myelin basic protein (MBP) expression, but an absence of myelin oligodendrocyte glycoprotein (MOG) in the murine esophagus. Selected immunohistochemistry for GFAP, PLP, and MBP including transgenic mice with cell-type specific expression of PLP and GFAP supported these results by detection of (1) GFAP, PLP, and MBP in Schwann cells in skeletal muscle and esophagus; (2) GFAP, PLP, but no MBP in perisynaptic Schwann cells of skeletal and esophageal motor endplates; (3) GFAP and PLP, but no MBP in glial cells surrounding esophageal myenteric neurons; and (4) PLP, but no GFAP and MBP in enteric glial cells forming a network in the esophagus. Our results pave the way for further investigations regarding the involvement of esophageal glial cells in the pathogenesis of dysphagia in MS. Full article
(This article belongs to the Special Issue CNS Drug Action in Neurodegenerative Diseases 2.0)
Show Figures

Graphical abstract

Back to TopTop