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Antioxidants
Special Issues
Redox Signaling in Brain Aging and Neurodegeneration
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Redox Signaling in Brain Aging and Neurodegeneration

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: 28 September 2025 | Viewed by 1326

Special Issue Editor

Dr. Marco Bisaglia

E-Mail Website
Guest Editor
Department of Biology, University of Padova, Via Ugo Bassi 58/B, 35131 Padova, Italy
Interests: neurodegenerative disease; mitochondrial dysfunction; oxidative stress; Parkinson’s diseases; molecular mechanisms
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Redox signaling is increasingly recognized as a critical factor in brain aging and neurodegenerative diseases. While physiological levels of reactive oxygen and nitrogen species serve as essential signaling molecules, their dysregulation contributes to oxidative stress, mitochondrial dysfunction, proteostasis defects, and neuroinflammation, ultimately leading to neuronal damage. Brain aging is characterized by a gradual decline in antioxidant defenses, rendering neural tissues more susceptible to redox imbalances. This vulnerability is further exacerbated in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis, where disrupted redox signaling intersects with proteostasis alteration, inflammation, and synaptic dysfunction.

This Special Issue explores the intricate mechanisms underlying redox signaling in brain aging and its transition to neurodegenerative states. Key topics include the role of redox-sensitive signaling pathways, the impact of oxidative damage on neuronal networks, and the therapeutic potential of targeting redox imbalance. By integrating insights from molecular biology, neuroscience, and translational research, this issue aims to advance our understanding of redox dynamics in brain health and disease, ultimately paving the way for innovative approaches to mitigate neurodegeneration and promote healthy aging.

Dr. Marco Bisaglia
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

  • aging
  • autophagy
  • brain
  • Alzheimer disease
  • amyotrophic lateral sclerosis
  • Friedreich ataxia
  • Huntington disease
  • neurodegeneration
  • oxidative stress
  • protein aggregation
  • Parkinson’s disease
  • reactive oxygen species

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Published Papers (2 papers)

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Research

15 pages, 1866 KiB  
Article
A High-Fat Diet Induces Oxidative Stress in OPA1+/− Mouse Cortices: A Critical Double Challenge
by Camille Champigny, Marlène Botella, Djamaa Atamena, Sébastien Bullich, Corentin Coustham, Bruno Guiard, Pascale Belenguer and Noélie Davezac
Antioxidants 2025, 14(7), 876; https://doi.org/10.3390/antiox14070876 - 17 Jul 2025
Viewed by 177
Abstract
A high-fat diet (HFD) has significant effects on health, leading to cardiovascular, metabolic, neurodegenerative, and psychiatric conditions and contributing to obesity and type 2 diabetes. Mitochondria, essential for energy production and oxidative metabolism, are adversely affected by a HFD, causing oxidative stress and [...] Read more.
A high-fat diet (HFD) has significant effects on health, leading to cardiovascular, metabolic, neurodegenerative, and psychiatric conditions and contributing to obesity and type 2 diabetes. Mitochondria, essential for energy production and oxidative metabolism, are adversely affected by a HFD, causing oxidative stress and impaired cellular function. Mutations in the OPA1 (OPtic Atrophy 1) gene, crucial for mitochondrial dynamics and functions, are responsible for dominant optic atrophy (DOA), a mitochondrial neurodegenerative disease associated with increased reactive oxygen species (ROS). The expressivity of DOA is highly variable, even within the same family. This suggests that both modifying genetics and environmental factors could influence the penetrance of the disease. We previously demonstrated that genetic background modulates DOA expressivity and now ask if this is also the case for external cues. We thus explore how OPA1 deficiency interacts with HFD-induced metabolic disturbances, hypothesizing that long-term HFD consumption impairs brain mitochondrial function and disrupts oxidative metabolism. OPA1+/− mice were thus subjected to a HFD for a period of 12 weeks, and ROS levels and the expression of antioxidant genes were evaluated by Western blot and spectrophotometry. Cortices from high-fat diet-fed OPA1+/− mice showed lower aconitase activity than those of their wild-type (WT) litter mates, indicative of an unbalanced increase in mitochondrial ROS. Accordingly, OPA1+/− mice present lower levels of the antioxidant enzyme superoxide dismutase 2 compared to WT mice. Therefore, this study (i) reveals the onset of oxidative stress in brain cortices from OPA1+/− mice challenged with a HFD, (ii) shows that diet is a modifying factor for DOA, and (iii) suggests that food control could be used to moderate the severity of the disease. Full article
(This article belongs to the Special Issue Redox Signaling in Brain Aging and Neurodegeneration)
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17 pages, 1096 KiB  
Article
Subchronic Intranasal Administration of NeuroEPO Reduces Long-Term Consequences of Severe Traumatic Brain Injury in Male Rats
by Félix Iván López-Preza, Maria de los Angeles Nuñez-Lumbreras, Iliana Sosa-Testé, Alonso Fernández-Guasti, Luis Concha, Teresita Rodríguez-Obaya and Luisa Rocha
Antioxidants 2025, 14(6), 710; https://doi.org/10.3390/antiox14060710 - 11 Jun 2025
Viewed by 899
Abstract
Current treatments fail to prevent long-term consequences induced by a severe traumatic brain injury (TBI). This study aimed to evaluate the efficacy of repetitive intranasal administration of NeuroEPO (a derivative of erythropoietin) on long-term alterations after a severe TBI induced by the application [...] Read more.
Current treatments fail to prevent long-term consequences induced by a severe traumatic brain injury (TBI). This study aimed to evaluate the efficacy of repetitive intranasal administration of NeuroEPO (a derivative of erythropoietin) on long-term alterations after a severe TBI induced by the application of a lateral fluid percussion in male rats. A otal of 30–31 days after the trauma, TBI+vehicle group showed sensorimotor dysfunction (Neuroscore, p < 0.0009; beam walking test, p < 0.0001 vs. Sham+vehicle group) and depressive-like behavior suggested by increased immobility (p = 0.0009 vs. baseline) during the forced swim test. Rats also showed increased production of malondialdehyde (a marker of oxidative damage), increased catalase activity (an antioxidant enzyme), and atrophy of brain areas evaluated with Magnetic Resonance Imaging 31 days after the trauma. TBI+NeuroEPO group received intranasal administration of NeuroEPO (0.136 mg/kg) starting 3 h post-TBI and continued every 8 h for four days. This group showed less sensorimotor dysfunction (Neuroscore, p = 0.020; beam walking test, p = 0.001, vs. TBI+vehicle group) and normal immobility behavior (p = 0.998 vs. Sham+vehicle group). Levels of malondialdehyde and catalase as well as the volume of brain structures of this group were like the Sham+vehicle group. These findings support the potential of NeuroEPO as a therapeutic agent to reduce long-term consequences of TBI. Full article
(This article belongs to the Special Issue Redox Signaling in Brain Aging and Neurodegeneration)
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