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Antioxidants
Special Issues
Oxidative Stress and Neuroinflammation in Neurodegenerative Diseases: Mechanisms and Therapies
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Oxidative Stress and Neuroinflammation in Neurodegenerative Diseases: Mechanisms and Therapies

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: 20 August 2024 | Viewed by 1406

Special Issue Editors

Prof. Dr. Ana M. Munoz

E-Mail Website
Guest Editor
1. Laboratory of Cell and Molecular Neurobiology of Parkinson's Disease, Department of Morphological Sciences, Research Center for Molecular Medicine and Chronic Diseases (CIMUS), IDIS, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain
2. Networking Research Center on Neurodegenerative Diseases (CIBERNED), 28029 Madrid, Spain
Interests: Parkinson's disease; dyskinesia; neurodegeneration; oxidative stress; neuroinflammation; neuroprotection
Dr. Jannette Rodríguez-Pallares

E-Mail Website
Guest Editor
1. Laboratory of Neuroanatomy and Experimental Neurology, Department of Morphological Sciences, CIMUS, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain
2. Networking Research Center on Neurodegenerative Diseases (CIBERNED), 28029 Madrid, Spain
Interests: neuroscience; neurodegeneration; neuroprotection; cell therapy; Parkinson's disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are the leading causes of disability and dependency, and the second leading cause of mortality worldwide. With the increase in life expectancy, the incidence of neurodegenerative diseases and their global socioeconomic impact has increased considerably in recent years and is expected to increase further in the coming decades. Aging is one of the main risk factors for these diseases, accelerating the cellular death process. It has been described that different neurodegenerative diseases have common mechanisms underlying neuronal death, even when the symptoms and the areas of the nervous system affected are different. Oxidative stress and chronic neuroinflammation are common pathological mechanisms in diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease, or amyotrophic lateral sclerosis. Microglia activation could induce the release of cytokines and an upregulated production of reactive oxygen species leading to mitochondrial dysfunction and neuronal death.  Nevertheless, the mechanisms involved in the different diseases are not fully understood. Consistent with this, strategies modulating oxidative stress and neuroinflammatory pathways are proposed as effective therapies to counteract the progression of neurodegeneration, and numerous assays in experimental models and clinical trials are carried out. However, there is still no effective therapy for these diseases, and many issues should be addressed.   

This Special Issue aims to publish original research studies or reviews to broaden the knowledge of the mechanisms related to oxidative stress and neuroinflammation in neurodegenerative diseases to develop new therapeutical approaches targeting these pathways.

We invite you to submit your contribution to this Special Issue, and we are highly grateful to receive your manuscripts.

Prof. Dr. Ana M. Munoz
Dr. Jannette Rodríguez-Pallares
Guest Editors

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

  • neurodegeneration
  • aging
  • neuroprotection
  • mitochondrial dysfunction
  • cytokines
  • apoptosis
  • autophagy
  • microglia
  • astroglia
  • antioxidants
  • free radicals

Published Papers (2 papers)

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16 pages, 2648 KiB  
Article
Selenium-Enriched E. coli Bacteria Mitigate the Age-Associated Degeneration of Cholinergic Neurons in C. elegans
by Palina Zytner, Anne Kutschbach, Weiye Gong, Verena Alexia Ohse, Laura Taudte, Anna Patricia Kipp, Lars-Oliver Klotz, Josephine Priebs and Holger Steinbrenner
Antioxidants 2024, 13(4), 492; https://doi.org/10.3390/antiox13040492 - 20 Apr 2024
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Abstract
Selenium (Se) is an essential trace element for humans and animals, but high-dose supplementation with Se compounds, most notably selenite, may exert cytotoxic and other adverse effects. On the other hand, bacteria, including Escherichia coli (E. coli), are capable of reducing [...] Read more.
Selenium (Se) is an essential trace element for humans and animals, but high-dose supplementation with Se compounds, most notably selenite, may exert cytotoxic and other adverse effects. On the other hand, bacteria, including Escherichia coli (E. coli), are capable of reducing selenite to red elemental Se that may serve as a safer Se source. Here, we examined how a diet of Se-enriched E. coli bacteria affected vital parameters and age-associated neurodegeneration in the model organism Caenorhabditis elegans (C. elegans). The growth of E. coli OP50 for 48 h in medium supplemented with 1 mM sodium selenite resulted in reddening of the bacterial culture, accompanied by Se accumulation in the bacteria. Compared to nematodes supplied with the standard E. coli OP50 diet, the worms fed on Se-enriched bacteria were smaller and slimmer, even though their food intake was not diminished. Nevertheless, given the choice, the nematodes preferred the standard diet. The fecundity of the worms was not affected by the Se-enriched bacteria, even though the production of progeny was somewhat delayed. The levels of the Se-binding protein SEMO-1, which serves as a Se buffer in C. elegans, were elevated in the group fed on Se-enriched bacteria. The occurrence of knots and ruptures within the axons of cholinergic neurons was lowered in aged nematodes provided with Se-enriched bacteria. In conclusion, C. elegans fed on Se-enriched E. coli showed less age-associated neurodegeneration, as compared to nematodes supplied with the standard diet. Full article
(This article belongs to the Special Issue Oxidative Stress and Neuroinflammation in Neurodegenerative Diseases: Mechanisms and Therapies)
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20 pages, 2192 KiB  
Article
Altered Brain Cholesterol Machinery in a Down Syndrome Mouse Model: A Possible Common Feature with Alzheimer’s Disease
by Erica Staurenghi, Gabriella Testa, Valerio Leoni, Rebecca Cecci, Lucrezia Floro, Serena Giannelli, Eugenio Barone, Marzia Perluigi, Gabriella Leonarduzzi, Barbara Sottero and Paola Gamba
Antioxidants 2024, 13(4), 435; https://doi.org/10.3390/antiox13040435 - 03 Apr 2024
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Abstract
Down syndrome (DS) is a complex chromosomal disorder considered as a genetically determined form of Alzheimer’s disease (AD). Maintenance of brain cholesterol homeostasis is essential for brain functioning and development, and its dysregulation is associated with AD neuroinflammation and oxidative damage. Brain cholesterol [...] Read more.
Down syndrome (DS) is a complex chromosomal disorder considered as a genetically determined form of Alzheimer’s disease (AD). Maintenance of brain cholesterol homeostasis is essential for brain functioning and development, and its dysregulation is associated with AD neuroinflammation and oxidative damage. Brain cholesterol imbalances also likely occur in DS, concurring with the precocious AD-like neurodegeneration. In this pilot study, we analyzed, in the brain of the Ts2Cje (Ts2) mouse model of DS, the expression of genes encoding key enzymes involved in cholesterol metabolism and of the levels of cholesterol and its main precursors and products of its metabolism (i.e., oxysterols). The results showed, in Ts2 mice compared to euploid mice, the downregulation of the transcription of the genes encoding the enzymes 3-hydroxy-3-methylglutaryl-CoA reductase and 24-dehydrocholesterol reductase, the latter originally recognized as an indicator of AD, and the consequent reduction in total cholesterol levels. Moreover, the expression of genes encoding enzymes responsible for brain cholesterol oxidation and the amounts of the resulting oxysterols were modified in Ts2 mouse brains, and the levels of cholesterol autoxidation products were increased, suggesting an exacerbation of cerebral oxidative stress. We also observed an enhanced inflammatory response in Ts2 mice, underlined by the upregulation of the transcription of the genes encoding for α-interferon and interleukin-6, two cytokines whose synthesis is increased in the brains of AD patients. Overall, these results suggest that DS and AD brains share cholesterol cycle derangements and altered oxysterol levels, which may contribute to the oxidative and inflammatory events involved in both diseases. Full article
(This article belongs to the Special Issue Oxidative Stress and Neuroinflammation in Neurodegenerative Diseases: Mechanisms and Therapies)
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