molecules-logo

Journal Browser

Journal Browser

Current and Novel Therapeutic Molecules for Treatment of Neuroinflammation-Mediated Neurodegenerative Disorders

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 2352

Special Issue Editor

Special Issue Information

Dear Colleagues,

Neuroinflammation is a defense mechanism that initially can have beneficial effects for the central nervous system (CNS), by removing or inhibiting diverse pathogens or cellular debris and promoting tissue repair. Sustained inflammatory responses, however, are detrimental, and they inhibit regeneration. Interestingly, neuroinflammation is emerging as a common feature to target in most CNS pathologies. Neuroinflammation is associated with various neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and others. The lack of effective treatments for most neurodegenerative diseases has prompted the search for novel therapeutic options.

Recent studies suggest the effectiveness of targeted delivery of small molecules to reduce neuroinflammation. A factor limiting the effectiveness of many pharmacological treatments is represented by the blood brain barrier which can lead to the suboptimal action of drugs in the CNS because the neurotherapeutic compounds are currently administered systemically without spatial or temporal control. Emerging technologies of new molecules, such as nanomaterials or small molecules, are providing promising tools to effectively access the brain in a targeted and controlled manner.

This special issue aims to collect current therapeutic options that have a significant impact in the treatment of inflammatory-based neurodegenerative diseases. A further goal is to review emerging therapies in clinical development, including agents that interfere with pathological processes deemed important for neurodegeneration or that aim to enhance reparative and neuroprotective responses. Finally, attention is paid to those studies aimed at identifying therapeutic drugs, small molecules and biological products that can modulate and control neuroinflammation.

Prof. Dr. Maria Antonietta Panaro
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. Molecules is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • brain
  • neuroinflammation
  • neurodegeneration
  • small-molecule therapeutics
  • bioactive compounds
  • natural products
  • drug development

Published Papers (1 paper)

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

Research

25 pages, 37983 KiB  
Article
Gastric Enteric Glial Cells: A New Contributor to the Synucleinopathies in the MPTP-Induced Parkinsonism Mouse
by Yang Heng, Yan-Yan Li, Lu Wen, Jia-Qing Yan, Nai-Hong Chen and Yu-He Yuan
Molecules 2022, 27(21), 7414; https://doi.org/10.3390/molecules27217414 - 01 Nov 2022
Cited by 1 | Viewed by 2045
Abstract
Accumulating evidence has shown that Parkinson’s disease (PD) is a systemic disease other than a mere central nervous system (CNS) disorder. One of the most important peripheral symptoms is gastrointestinal dysfunction. The enteric nervous system (ENS) is regarded as an essential gateway to [...] Read more.
Accumulating evidence has shown that Parkinson’s disease (PD) is a systemic disease other than a mere central nervous system (CNS) disorder. One of the most important peripheral symptoms is gastrointestinal dysfunction. The enteric nervous system (ENS) is regarded as an essential gateway to the environment. The discovery of the prion-like behavior of α-synuclein makes it possible for the neurodegenerative process to start in the ENS and spread via the gut-brain axis to the CNS. We first confirmed that synucleinopathies existed in the stomachs of chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)/probenecid (MPTP/p)-induced PD mice, as indicated by the significant increase in abnormal aggregated and nitrated α-synuclein in the TH-positive neurons and enteric glial cells (EGCs) of the gastric myenteric plexus. Next, we attempted to clarify the mechanisms in single MPTP-injected mice. The stomach naturally possesses high monoamine oxidase-B (MAO-B) activity and low superoxide dismutase (SOD) activity, making the stomach susceptible to MPTP-induced oxidative stress, as indicated by the significant increase in reactive oxygen species (ROS) in the stomach and elevated 4-hydroxynonenal (4-HNE) in the EGCs after MPTP exposure for 3 h. Additionally, stomach synucleinopathies appear before those of the nigrostriatal system, as determined by Western blotting 12 h after MPTP injection. Notably, nitrated α-synuclein was considerably increased in the EGCs after 3 h and 12 h of MPTP exposure. Taken together, our work demonstrated that the EGCs could be new contributors to synucleinopathies in the stomach. The early-initiated synucleinopathies might further influence neighboring neurons in the myenteric plexus and the CNS. Our results offer a new experimental clue for interpreting the etiology of PD. Full article
Show Figures

Figure 1

Back to TopTop