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Oxidative and Redox Signalling in Neurological Diseases
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Oxidative and Redox Signalling in Neurological Diseases

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 28 February 2027 | Viewed by 10845

Editor

Dr. Malamati Kourti

E-Mail Website
Guest Editor
Department of Life Sciences, School of Sciences, European University Cyprus, 6 Diogenis Str., Nicosia 1516, Cyprus
Interests: oxidative stress; antioxidants; cancer; angiogenesis; carbon monoxide-releasing molecules
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue in the International Journal of Molecular Sciences will explore the expanding role of gasotransmitters—namely nitric oxide (NO), carbon monoxide (CO), and hydrogen sulphide (H₂S)—in the pathophysiology of neurological diseases, with particular emphasis on their modulation of oxidative and redox signalling pathways. These endogenous gaseous molecules have emerged as critical regulators of redox signalling, mitochondrial dynamics, neuroinflammation, and cell survival, all of which are fundamental to the onset and progression of a wide array of neurological disorders.

The Issue aims to provide a comprehensive platform for high-impact research that bridges basic science with translational perspectives, highlighting how the modulation of gasotransmitter pathways could lead to novel therapeutic strategies. It will welcome contributions addressing both acute (e.g., stroke, traumatic brain injury) and chronic (e.g., Alzheimer’s disease, Parkinson’s disease, multiple sclerosis) neurological conditions.

Topics for this Special Issue may include, but are not limited to, the following:

  • Molecular Mechanisms: The roles of NO, CO, and H₂S in redox homeostasis, oxidative/nitrosative stress, and neuronal signalling in health and disease;
  • Neurodegeneration and Aging: How gasotransmitter dysregulation contributes to aging-related neurodegenerative diseases such as Alzheimer's, Parkinson’s, and ALS, particularly through oxidative stress pathways;
  • Inflammation and Immunity: Interactions between gasotransmitters and neuroinflammatory processes, including the modulation of microglial and astrocytic activity;
  • Mitochondrial Function and Apoptosis: The impact of gasotransmitters on mitochondrial biogenesis, mitophagy, calcium signalling, and neuronal apoptosis under oxidative stress conditions;
  • Therapeutic Development: Advances in the design and delivery of gasotransmitter donors, inhibitors, and releasing molecules for intervention in oxidative stress-mediated neurological disorders;
  • Neurological Disorders Beyond Alzheimer’s: The exploration of gasotransmitter roles in epilepsy, ischemic injury, Huntington’s disease, multiple sclerosis, psychiatric conditions (e.g., depression, schizophrenia) with oxidative stress components, and peripheral nervous system diseases (e.g., neuropathic pain), where gasotransmitters play emerging roles;
  • Preclinical and Clinical Research: Translational studies evaluating the safety, efficacy, and mechanistic underpinnings of gasotransmitter-based therapies in neurological settings;
  • Biomarkers and Imaging: The development and validation of gasotransmitter-associated biomarkers for diagnosis, prognosis, and therapeutic monitoring in neurological diseases;
  • Vascular Contributions to Neurological Disorders: Gasotransmitters are key modulators of vascular tone and cerebral blood flow;
  • Glial Biology and Signalling: Gasotransmitters modulate astrocytes and microglia under oxidative stress;
  • Comparative Biology: Studies using animal models to investigate evolutionarily conserved gasotransmitter functions.

This broadened scope is intended to attract interdisciplinary submissions from neuroscience, pharmacology, medicinal chemistry, and clinical neurology, enhancing the visibility and impact of the Special Issue.

Dr. Malamati Kourti
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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

  • gasotransmitters
  • neurological diseases
  • oxidative stress
  • redox signalling
  • reactive oxygen species (ROS)
  • neuroinflammation
  • mitochondrial dysfunction
  • cell death/apoptosis
  • nitrosative stress
  • endogenous gas signalling
  • neuromodulation
  • neurovascular coupling
  • therapeutic strategies
  • biomarkers

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Published Papers (4 papers)

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Research

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22 pages, 8430 KB  
Article
Hyperbaric Oxygen Attenuates Cerebral Ischemia–Reperfusion Injury Through ROS-Dependent Remodeling of Microglial Mitochondrial Dynamics
by Haotian Wei, Xingyue Du, Shushu Xu, Qiuli Bo, Yanan Guo, Lihua Xu, Zhenglin Jiang, Xia Li and Yuan Yuan
Int. J. Mol. Sci. 2026, 27(14), 6334; https://doi.org/10.3390/ijms27146334 - 16 Jul 2026
Viewed by 632
Abstract
Hyperbaric oxygen (HBO) shows neuroprotective potential in cerebral ischemia–reperfusion (CIR) injury, but its variable efficacy suggests that the underlying cellular mechanisms remain incompletely defined. We previously showed that HBO suppresses microglial NLRP3 inflammasome activation after CIR injury in a reactive oxygen species (ROS)-dependent [...] Read more.
Hyperbaric oxygen (HBO) shows neuroprotective potential in cerebral ischemia–reperfusion (CIR) injury, but its variable efficacy suggests that the underlying cellular mechanisms remain incompletely defined. We previously showed that HBO suppresses microglial NLRP3 inflammasome activation after CIR injury in a reactive oxygen species (ROS)-dependent manner; yet, how ROS couples to this effect remains unclear. Since mitochondria regulate ROS and inflammasome signaling, we investigated whether HBO modulates microglial mitochondrial dynamics in CIR injury. In adult male ICR mice (n = 71, 8–12 weeks) subjected to 60 min middle cerebral artery occlusion followed by 24 h reperfusion, HBO improved neurological function, reduced infarct area, and decreased ASC-positive microglia/macrophages. In lipopolysaccharide/nigericin-stimulated primary microglia, HBO suppressed IL-1β release, reduced mitochondrial fragmentation, preserved mitochondrial membrane potential, maintained mitofusin 2 (MFN2) protein level, and reduced DRP1 Ser616 phosphorylation without altering total DRP1 or FIS1 expression. MitoTEMPOL abolished HBO-mediated protection against mitochondrial fragmentation, MFN2 reduction, and DRP1 Ser616 phosphorylation in vitro. Edaravone, when combined with HBO, attenuated HBO-mediated neuroprotection and counteracted HBO-induced regulation of MFN2 and DRP1 Ser616 phosphorylation in vivo. These findings support ROS-dependent remodeling of microglial mitochondrial dynamics as a mechanism contributing to HBO-mediated suppression of inflammasome-associated inflammation after CIR injury. Full article
(This article belongs to the Special Issue Oxidative and Redox Signalling in Neurological Diseases)
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Review

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27 pages, 2494 KB  
Review
The Emerging Role of Dimethyl Fumarate in Alzheimer’s Disease—A Systematic Review of Available Preclinical Studies
by Maria Mouaimi, Athanasios Metaxas and Malamati Kourti
Int. J. Mol. Sci. 2026, 27(10), 4227; https://doi.org/10.3390/ijms27104227 - 9 May 2026
Viewed by 913
Abstract
Dimethyl fumarate (DMF), a fumaric acid ester, is approved for psoriasis and multiple sclerosis due to its antioxidant and anti-inflammatory properties mediated via Nrf2 activation. Nrf2 regulates genes that protect cells from oxidative stress, a key factor in neurodegenerative diseases such as Alzheimer’s [...] Read more.
Dimethyl fumarate (DMF), a fumaric acid ester, is approved for psoriasis and multiple sclerosis due to its antioxidant and anti-inflammatory properties mediated via Nrf2 activation. Nrf2 regulates genes that protect cells from oxidative stress, a key factor in neurodegenerative diseases such as Alzheimer’s disease (AD), which is characterized by amyloid-β and tau accumulation and lipid peroxidation. This systematic review aimed to evaluate preclinical evidence for DMF as a potential therapeutic agent in AD models through Nrf2 activation. A comprehensive literature search of PubMed and Scopus (last search: December 2025) identified in vitro, in vivo, and combined preclinical studies assessing DMF in AD models. Studies were screened using predefined inclusion and exclusion criteria, and methodological quality was assessed using established tools. Results were synthesized narratively. Eighteen studies were ultimately included in the analysis. Across the included studies, DMF consistently activated the Nrf2 pathway, enhancing antioxidant and anti-inflammatory gene expression. DMF treatment reduced amyloid-β and tau protein levels, mitigated oxidative stress, and improved cognitive performance in animal models. However, the evidence is limited by heterogeneity in experimental models and methodological variability. In conclusion, preclinical evidence suggests DMF is a promising candidate for AD treatment by targeting oxidative stress and neuroinflammation via Nrf2 activation. Further preclinical studies, particularly on ferroptosis mechanisms, and well-designed clinical studies are warranted to clarify its full therapeutic potential. This review was not registered and the authors received no funding. Full article
(This article belongs to the Special Issue Oxidative and Redox Signalling in Neurological Diseases)
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34 pages, 770 KB  
Review
Shared Neuroinflammatory Mechanisms Across Dementia Types: An Integrative Review
by Subramanian Thangaleela, Asif Ali, Yohanes Tandoro and Chin-Kun Wang
Int. J. Mol. Sci. 2026, 27(1), 179; https://doi.org/10.3390/ijms27010179 - 23 Dec 2025
Cited by 4 | Viewed by 2732
Abstract
Dementia is a neurodegenerative condition marked by progressive cognitive decline, which affects people worldwide. Studies on dementia typically continue over years of uncertainty. Different types of dementia, like Alzheimer’s disease dementia, Lewy body dementia, frontotemporal dementia, and vascular dementia, exhibit different pathological features, [...] Read more.
Dementia is a neurodegenerative condition marked by progressive cognitive decline, which affects people worldwide. Studies on dementia typically continue over years of uncertainty. Different types of dementia, like Alzheimer’s disease dementia, Lewy body dementia, frontotemporal dementia, and vascular dementia, exhibit different pathological features, yet their downstream inflammatory pathways involve similar inflammatory mediators. As an initial trigger, microglial cells and astrocytes become activated by protein aggregates, mutations, or any other cause, and release pro-inflammatory cytokines, which can lead to synaptic dysfunction, neuronal degeneration, and impaired cognitive function. Neuroinflammation plays a critical role in the pathogenesis of all forms of dementia. Despite their distinct neuropathological features, inflammatory processes may coincide at a point and lead to neuronal degeneration and cognitive decline. Recent advancements in neuroimaging techniques and biomarker discovery revealed potential therapeutic targets that may mitigate neuroinflammation. The primary objective of this review is to explore the underlying mechanisms linking neuroinflammation to various types of dementia. This review focuses on shared and distinct neuroinflammatory mechanisms to unravel significant therapeutic strategies for dementia. Full article
(This article belongs to the Special Issue Oxidative and Redox Signalling in Neurological Diseases)
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22 pages, 2302 KB  
Review
Organophosphate Chemical Nerve Agents, Oxidative Stress, and NADPH Oxidase Inhibitors: An Overview
by Christina Meyer and Thimmasettappa Thippeswamy
Int. J. Mol. Sci. 2025, 26(19), 9313; https://doi.org/10.3390/ijms26199313 - 24 Sep 2025
Cited by 8 | Viewed by 5883
Abstract
Organophosphates (OPs) are potent anti-acetylcholinesterase compounds historically used as pesticides and exploited in chemical warfare. Exposure to OPs initiates cholinergic crisis with both peripheral and central effects such as salivation, lacrimation, urination, and defecation (SLUD), and status epilepticus (SE), a prolonged state of [...] Read more.
Organophosphates (OPs) are potent anti-acetylcholinesterase compounds historically used as pesticides and exploited in chemical warfare. Exposure to OPs initiates cholinergic crisis with both peripheral and central effects such as salivation, lacrimation, urination, and defecation (SLUD), and status epilepticus (SE), a prolonged state of seizure. Standard medical countermeasures atropine, oximes, and benzodiazepines reduce mortality, control peripheral symptoms, and terminate SE. However, they do not attenuate the consequences of SE, including neurodegeneration, oxidative stress, neuroinflammation, epilepsy, and associated comorbidities such as cognitive dysfunction. SE induces excessive NADPH oxidase (NOX) synthesis and production of reactive oxygen species, which is a key driver of neurodegeneration and epilepsy. Furthermore, inhibition of NOX in SE-induced epilepsy models reduces neuroinflammation, neurodegeneration, and seizure frequency. Following OP toxicity, treatment with NOX inhibitors diapocynin and mitoapocynin reduced oxidative stress and astrocyte reactivity. This review summarizes the history and development of OPs and the current knowledge on OP toxicity, emphasizing the role of NOX, and the therapeutic potential of NOX inhibitors in treating long-term consequences of acute exposure to OPs. Full article
(This article belongs to the Special Issue Oxidative and Redox Signalling in Neurological Diseases)
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