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Biomolecules
Special Issues
Molecular Mechanisms and Pharmacological Target of Neuroprotection
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Molecular Mechanisms and Pharmacological Target of Neuroprotection

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (20 April 2024) | Viewed by 7585

Special Issue Editor

Dr. Zhidong Zhou

E-Mail Website
Guest Editor
Translational Therapeutics Laboratory, Duke-NUS Graduate Medical School, NBD, Level 6, 8 College Road, Singapore 169857, Singapore
Interests: biomarkers; therapeutic targets and compounds for Parkinson’s disease and other neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

I am pleased to invite you to make your contributions to this Special Issue, titled "Molecular Mechanisms and Therapeutic Targets of Neuroprotection".

So far, a wide spectrum of neurodegenerative diseases has been found to affect the central and peripheral nervous systems of millions of people worldwide. These formidable and incurable chronic disorders include Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple system atrophy, amyotrophic lateral sclerosis, and other motor neuron diseases. Among these diseases, Alzheimer’s disease and Parkinson’s disease are the two most common neurodegenerative disorders. The onset and progression of neurodegenerative diseases can be induced by the impairment, degeneration, and demise of neurons in the brain and spinal cords of the subjects diagnosed with these diseases. The degeneration of the neurons in the human nervous system can impact many aspects of the human body, including balance, movement, talking, breathing, and memory and can even enhance the mortality of these patients. Many of these diseases can be caused by genetic factors. However, adverse environmental factors can also contribute to neurodegeneration. Although considerable discoveries have been achieved by researchers worldwide, the pathogenesis of neurodegeneration is still unclear, and no therapeutic strategies or drugs can stop or alleviate the progressive neurodegeneration in the brain and spinal cords of the affected patients.

This Special Issue will focus on the molecular mechanisms and therapeutic targets of neuroprotection. Novel findings on key therapeutic targets and underlying molecular mechanisms will help us to develop new therapeutic strategies and agents to treat neurodegeneration and benefit our patients. In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Studies on biomarkers or therapeutic targets of neurodegeneration;
  • Cellular and molecular pathogenesis of neurodegeneration;
  • High-throughput screening for neuroprotective compounds or drugs;
  • In vitro and in vivo disease models of neurodegenerative diseases;
  • Studies on protection and underlying mechanisms of neuroprotective compounds;
  • System biological studies on disease pathogenesis and neuroprotection;
  • Clinical trials on new neuroprotective drugs;
  • Multidisciplinary studies on neuroprotection and mechanisms.

I/We look forward to receiving your contributions.

Dr. Zhidong Zhou
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. Biomolecules is an international peer-reviewed open access monthly 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

  • neurodegenerative disease
  • neuroprotection
  • pathogenesis
  • therapeutic agents
  • therapeutic targets

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Published Papers (4 papers)

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Research

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15 pages, 4706 KiB  
Article
Comparative Study of the Protective and Neurotrophic Effects of Neuronal and Glial Progenitor Cells-Derived Conditioned Media in a Model of Glutamate Toxicity In Vitro
by Georgy Leonov, Diana Salikhova, Margarita Shedenkova, Tatiana Bukharova, Timur Fatkhudinov and Dmitry Goldshtein
Biomolecules 2023, 13(12), 1784; https://doi.org/10.3390/biom13121784 - 13 Dec 2023
Cited by 3 | Viewed by 1667
Abstract
Cell therapy represents a promising approach to the treatment of neurological diseases, offering potential benefits not only by cell replacement but also through paracrine secretory activities. However, this approach includes a number of limiting factors, primarily related to safety. The use of conditioned [...] Read more.
Cell therapy represents a promising approach to the treatment of neurological diseases, offering potential benefits not only by cell replacement but also through paracrine secretory activities. However, this approach includes a number of limiting factors, primarily related to safety. The use of conditioned stem cell media can serve as an equivalent to cell therapy while avoiding its disadvantages. The present study was a comparative investigation of the antioxidant, neuroprotective and neurotrophic effects of conditioned media obtained from neuronal and glial progenitor cells (NPC-CM and GPC-CM) on the PC12 cell line in vitro. Neuronal and glial progenitor cells were obtained from iPSCs by directed differentiation using small molecules. GPC-CM reduced apoptosis, ROS levels and increased viability, expressions of the antioxidant response genes HMOX1 and NFE2L2 in a model of glutamate-induced oxidative stress. The neurotrophic effect was evidenced by a change in the morphology of pheochromocytoma cells to a neuron-like phenotype. Moreover, neurite outgrowth, expression of GAP43, TUBB3, MAP2, SYN1 genes and increased levels of the corresponding MAP2 and TUBB3 proteins. Treatment with NPC-CM showed moderate antiapoptotic effects and improved cell viability. This study demonstrated the potential application of CM in the field of regenerative medicine. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pharmacological Target of Neuroprotection)
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14 pages, 1909 KiB  
Article
Thiazole Derivatives as Modulators of GluA2 AMPA Receptors: Potent Allosteric Effects and Neuroprotective Potential
by Mohammed Hawash
Biomolecules 2023, 13(12), 1694; https://doi.org/10.3390/biom13121694 - 23 Nov 2023
Cited by 4 | Viewed by 1314
Abstract
Thiazole carboxamide derivatives were synthesized in this investigation, with a subsequent examination of their impact on GluA2 AMPA receptors. The synthesized compounds, namely MMH-1-5, were subjected to characterization using high-resolution mass spectrometry (HRMS), proton nuclear magnetic resonance (1H-NMR), and carbon-13 nuclear [...] Read more.
Thiazole carboxamide derivatives were synthesized in this investigation, with a subsequent examination of their impact on GluA2 AMPA receptors. The synthesized compounds, namely MMH-1-5, were subjected to characterization using high-resolution mass spectrometry (HRMS), proton nuclear magnetic resonance (1H-NMR), and carbon-13 nuclear magnetic resonance (13C-NMR). The present work thoroughly investigates the impact of five thiazole derivatives on GluA2 AMPA receptors. This investigation examined their effects on both whole-cell currents and receptor kinetics. In addition, the cytotoxicity of the samples was assessed using the MTS test. The compound MMH-5 had the highest effect level, resulting in a notable drop in current amplitude by a factor of six. Similarly, MMH-4 and MMH-3 also caused major reductions in the current amplitude. The compounds mentioned above also influenced the rates of deactivation and desensitization. MMH-5 and MMH-4 exhibited an increase in deactivation, while MMH-5 showed reduced desensitization. Our research findings highlight the efficacy of MMH-5 as a negative allosteric modulator of GluA2 AMPA receptors, exerting substantial effects on both the magnitude and time course of receptor activity. Significantly, the compound MMH-2 demonstrated noteworthy cytotoxic effects, as evidenced by cell viability rates dropping below 6.79% for all cancer cell lines and 17.52% for the normal cell line (LX-2). Of particular interest is the pronounced cytotoxicity observed in MMH-5, suggesting its potential as a safe neuroprotective agent targeting the AMPA receptor, as indicated by cell viability percentages exceeding 85.44% across all cancer and normal cell lines. Docking simulations were performed to determine possible modes of interaction between MMH5 and the GluA2-AMPA receptor (PDB:7RZ5). The abovementioned facts and the well-documented effects of further thiazole derivatives provide a strong foundation for future research endeavors to enhance tailored treatments for neurological disorders that rely heavily on GluA2 signaling. The present study elucidates the intricate association between thiazole derivatives and GluA2 receptors, providing valuable perspectives on the prospects of enhanced and specific therapeutic interventions for diverse neurological conditions. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pharmacological Target of Neuroprotection)
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Review

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12 pages, 1114 KiB  
Review
Molecular Interactions between Neuroglobin and Cytochrome c: Possible Mechanisms of Antiapoptotic Defense in Neuronal Cells
by Marina A. Semenova, Rita V. Chertkova, Mikhail P. Kirpichnikov and Dmitry A. Dolgikh
Biomolecules 2023, 13(8), 1233; https://doi.org/10.3390/biom13081233 - 10 Aug 2023
Cited by 2 | Viewed by 1616
Abstract
Neuroglobin, which is a heme protein from the globin family that is predominantly expressed in nervous tissue, can promote a neuronal survivor. However, the molecular mechanisms underlying the neuroprotective function of Ngb remain poorly understood to this day. The interactions between neuroglobin and [...] Read more.
Neuroglobin, which is a heme protein from the globin family that is predominantly expressed in nervous tissue, can promote a neuronal survivor. However, the molecular mechanisms underlying the neuroprotective function of Ngb remain poorly understood to this day. The interactions between neuroglobin and mitochondrial cytochrome c may serve as at least one of the mechanisms of neuroglobin-mediated neuroprotection. Interestingly, neuroglobin and cytochrome c possibly can interact with or without electron transfer both in the cytoplasm and within the mitochondria. This review provides a general picture of molecular interactions between neuroglobin and cytochrome c based on the recent experimental and computational work on neuroglobin and cytochrome c interactions. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pharmacological Target of Neuroprotection)
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Other

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21 pages, 1500 KiB  
Systematic Review
Circular RNAs in Ischemic Stroke: Biological Role and Experimental Models
by Chiara Siracusa, Jolanda Sabatino, Isabella Leo, Ceren Eyileten, Marek Postuła and Salvatore De Rosa
Biomolecules 2023, 13(2), 214; https://doi.org/10.3390/biom13020214 - 22 Jan 2023
Cited by 10 | Viewed by 2358
Abstract
Ischemic stroke is among the leading causes of morbidity, disability, and mortality worldwide. Despite the recent progress in the management of acute ischemic stroke, timely intervention still represents a challenge. Hence, strategies to counteract ischemic brain injury during and around the acute event [...] Read more.
Ischemic stroke is among the leading causes of morbidity, disability, and mortality worldwide. Despite the recent progress in the management of acute ischemic stroke, timely intervention still represents a challenge. Hence, strategies to counteract ischemic brain injury during and around the acute event are still lacking, also due to the limited knowledge of the underlying mechanisms. Despite the increasing understanding of the complex pathophysiology underlying ischemic brain injury, some relevant pieces of information are still required, particularly regarding the fine modulation of biological processes. In this context, there is emerging evidence that the modulation of circular RNAs, a class of highly conserved non-coding RNA with a closed-loop structure, are involved in pathophysiological processes behind ischemic stroke, unveiling a number of potential therapeutic targets and possible clinical biomarkers. This paper aims to provide a comprehensive overview of experimental studies on the role of circular RNAs in ischemic stroke. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pharmacological Target of Neuroprotection)
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