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Antioxidants
Special Issues
Redox Signaling Regulation in Neurological Disorders
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Redox Signaling Regulation in Neurological Disorders

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 May 2023) | Viewed by 11843

Special Issue Editor

Dr. Susana Solá

E-Mail Website
Guest Editor
Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, 1649-003 Lisbon, Portugal
Interests: aging; bioenergetics; cell signaling; mitochondrial metabolism; neural stem cell fate; neuroregeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The brain is one of the most metabolically active organs in the human body. The vast majority of neurological disorders are somehow related to disturbed energetic problems and/or the mechanisms by which neural cells handle their own, or surrounding, waste metabolites. Adult neural stem cells (NSCs) play a key role in regulating brain rejuvenation and plasticity in mature brains. Recent evidence reveals that these cells are also pivotal to buffer stress responses and depressive behavior. Notably, recent evidence has shown that NSCs modulate the viability and plasticity of neighboring cells, through a paracrine-mediated mechanism, allowing them to deliver efficient protective molecules through their secretome, and that redox oxidative signaling plays a key role in this process. Therefore, a better understanding of the redox mechanisms and redox-based therapeutic approaches for neuroprotection and regeneration will surely provide significant information for this field of study and allow for the design of more efficient and less-invasive strategies capable of boosting neuroplasticity throughout life.

We invite investigators to contribute original studies and review articles that clarify the redox regulation mechanisms in neurological disorders in order to envision the functional compensation of these signaling pathways during aging and prevent the onset of neurological disorders. We are interested in articles from basic research to clinical applications on different types of cells and organism models.

Dr. Susana Solá
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. Antioxidants 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 2900 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

  • redox signaling
  • neural stem cells
  • metabolism
  • neurodegeneration
  • neurodegeneration
  • neurological disorders

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Published Papers (3 papers)

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Review

34 pages, 1855 KiB  
Review
Redox Imbalance in Neurological Disorders in Adults and Children
by Federica Rey, Clarissa Berardo, Erika Maghraby, Alessia Mauri, Letizia Messa, Letizia Esposito, Giovanna Casili, Sara Ottolenghi, Eleonora Bonaventura, Salvatore Cuzzocrea, Gianvincenzo Zuccotti, Davide Tonduti, Emanuela Esposito, Irene Paterniti, Cristina Cereda and Stephana Carelli
Antioxidants 2023, 12(4), 965; https://doi.org/10.3390/antiox12040965 - 20 Apr 2023
Cited by 6 | Viewed by 4573
Abstract
Oxygen is a central molecule for numerous metabolic and cytophysiological processes, and, indeed, its imbalance can lead to numerous pathological consequences. In the human body, the brain is an aerobic organ and for this reason, it is very sensitive to oxygen equilibrium. The [...] Read more.
Oxygen is a central molecule for numerous metabolic and cytophysiological processes, and, indeed, its imbalance can lead to numerous pathological consequences. In the human body, the brain is an aerobic organ and for this reason, it is very sensitive to oxygen equilibrium. The consequences of oxygen imbalance are especially devastating when occurring in this organ. Indeed, oxygen imbalance can lead to hypoxia, hyperoxia, protein misfolding, mitochondria dysfunction, alterations in heme metabolism and neuroinflammation. Consequently, these dysfunctions can cause numerous neurological alterations, both in the pediatric life and in the adult ages. These disorders share numerous common pathways, most of which are consequent to redox imbalance. In this review, we will focus on the dysfunctions present in neurodegenerative disorders (specifically Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis) and pediatric neurological disorders (X-adrenoleukodystrophies, spinal muscular atrophy, mucopolysaccharidoses and Pelizaeus–Merzbacher Disease), highlighting their underlining dysfunction in redox and identifying potential therapeutic strategies. Full article
(This article belongs to the Special Issue Redox Signaling Regulation in Neurological Disorders)
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29 pages, 4289 KiB  
Review
Cell Rearrangement and Oxidant/Antioxidant Imbalance in Huntington’s Disease
by Francesco D’Egidio, Vanessa Castelli, Annamaria Cimini and Michele d’Angelo
Antioxidants 2023, 12(3), 571; https://doi.org/10.3390/antiox12030571 - 24 Feb 2023
Cited by 17 | Viewed by 2694
Abstract
Huntington’s Disease (HD) is a hereditary neurodegenerative disorder caused by the expansion of a CAG triplet repeat in the HTT gene, resulting in the production of an aberrant huntingtin (Htt) protein. The mutant protein accumulation is responsible for neuronal dysfunction and cell death. [...] Read more.
Huntington’s Disease (HD) is a hereditary neurodegenerative disorder caused by the expansion of a CAG triplet repeat in the HTT gene, resulting in the production of an aberrant huntingtin (Htt) protein. The mutant protein accumulation is responsible for neuronal dysfunction and cell death. This is due to the involvement of oxidative damage, excitotoxicity, inflammation, and mitochondrial impairment. Neurons naturally adapt to bioenergetic alteration and oxidative stress in physiological conditions. However, this dynamic system is compromised when a neurodegenerative disorder occurs, resulting in changes in metabolism, alteration in calcium signaling, and impaired substrates transport. Thus, the aim of this review is to provide an overview of the cell’s answer to the stress induced by HD, focusing on the role of oxidative stress and its balance with the antioxidant system. Full article
(This article belongs to the Special Issue Redox Signaling Regulation in Neurological Disorders)
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35 pages, 797 KiB  
Review
Potential Utility of Natural Products against Oxidative Stress in Animal Models of Multiple Sclerosis
by Zheng Zha, Sisi Liu, Yijiang Liu, Chen Li and Lei Wang
Antioxidants 2022, 11(8), 1495; https://doi.org/10.3390/antiox11081495 - 29 Jul 2022
Cited by 13 | Viewed by 3957
Abstract
Multiple sclerosis (MS) is an autoimmune-mediated degenerative disease of the central nervous system (CNS) characterized by immune cell infiltration, demyelination and axonal injury. Oxidative stress-induced inflammatory response, especially the destructive effect of immune cell-derived free radicals on neurons and oligodendrocytes, is crucial in [...] Read more.
Multiple sclerosis (MS) is an autoimmune-mediated degenerative disease of the central nervous system (CNS) characterized by immune cell infiltration, demyelination and axonal injury. Oxidative stress-induced inflammatory response, especially the destructive effect of immune cell-derived free radicals on neurons and oligodendrocytes, is crucial in the onset and progression of MS. Therefore, targeting oxidative stress-related processes may be a promising preventive and therapeutic strategy for MS. Animal models, especially rodent models, can be used to explore the in vivo molecular mechanisms of MS considering their similarity to the pathological processes and clinical signs of MS in humans and the significant oxidative damage observed within their CNS. Consequently, these models have been used widely in pre-clinical studies of oxidative stress in MS. To date, many natural products have been shown to exert antioxidant effects to attenuate the CNS damage in animal models of MS. This review summarized several common rodent models of MS and their association with oxidative stress. In addition, this review provides a comprehensive and concise overview of previously reported natural antioxidant products in inhibiting the progression of MS. Full article
(This article belongs to the Special Issue Redox Signaling Regulation in Neurological Disorders)
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