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Antioxidants
Special Issues
Natural Antioxidants in Neurodegeneration and Aging Processes
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Natural Antioxidants in Neurodegeneration and Aging Processes

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Natural and Synthetic Antioxidants".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 4611

Special Issue Editors

Prof. Dr. Uwe Wenzel

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Guest Editor
Molecular Nutrition Research, Interdisciplinary Research Centre, Justus Liebig University Giessen, Giessen, Germany
Interests: secondary plant compounds; neurodegenrative diseases; Alzheimers disease; proteostasis; mitophagy
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Edward J. Calabrese

E-Mail Website
Guest Editor
Department of Environmental Health Sciences, Morrill I, N344, University of Massachusetts, Amherst, MA 01003, USA
Interests: Oxidative stress, nutritional antioxidants, vitagenes, brain resilience, hormesis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Vittorio Calabrese

E-Mail Website
Guest Editor
Department of Biological and Biotechnological Sciences, Section of Medical Biochemistry, University of Catania, 95125 Catania, Italy
Interests: oxidative stress; nutritional antioxidants; vitagenes; brain resilience; hormesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer´s disease is a progressive neurodegenerative disorder representing the leading cause of dementia worldwide. The disease is characterized by the accumulation of senile plaques in the brain consisting mainly of amyloid-β. Oxidative stress plays a crucial role in the pathogenesis insofar as it leads to the functional impairment of cellular proteins and protein aggregation, resulting finally in the disturbance of the protein quality control, i.e., the proteostasis network. The efficiency of compensating mechanisms might determine the rapidity of disease progression. Those mechanisms encompass both the heat-shock response and unfolded protein response, but also protein degradation by the ubiquitin-proteasome system or by autophagy. At a higher level, all those processes might interfere with the functionality of mitochondria, responsible for energy generation and deciding between neuronal survival or programmed cell death. Accordingly, mitochondrial homoeostasis as defined by the rates of fusion, fission, mitophagy and mitochondrial biogenesis have a high impact on neuronal functionality and thus on the prevention or development of Alzheimer´s disease.  

As guest editors, we invite you to contribute to this Special Issue, whose focus will be the role of oxidative stress and antioxidants in the pathogenesis of Alzheimer´s disease and its prevention. Emphasis should be put on the proteostasis network and/or mitochondrial dynamics and functionality as affected by oxidants/antioxidants. We are also particularly interested in papers that explore how the concept of hormesis may affect public health strategies that prevent and/or slow the onset and reduce the severity of Alzheimer’s disease.

Prof. Dr. Uwe Wenzel
Prof. Dr. Edward J. Calabrese
Prof. Dr. Vittorio Calabrese
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

  • Alzheimer´s disease
  • antioxidants
  • proteostasis
  • hormesis
  • heat-shock response
  • unfolded protein response
  • mitochondrial dynamics
  • mitochondrial functionality

Published Papers (2 papers)

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Research

15 pages, 2913 KiB  
Article
Chronodisruption and Loss of Melatonin Rhythm, Associated with Alterations in Daily Motor Activity and Mitochondrial Dynamics in Parkinsonian Zebrafish, Are Corrected by Melatonin Treatment
by Paula Aranda-Martínez, José Fernández-Martínez, Yolanda Ramírez-Casas, César Rodríguez-Santana, Iryna Rusanova, Germaine Escames and Darío Acuña-Castroviejo
Antioxidants 2023, 12(4), 954; https://doi.org/10.3390/antiox12040954 - 18 Apr 2023
Cited by 4 | Viewed by 1606
Abstract
Beyond sleep/wake, clock genes regulate the daily rhythms of melatonin production, motor activity, innate immunity, and mitochondrial dynamics, among others. All these rhythms are affected in Parkinson’s disease (PD), suggesting that chronodisruption may be an early stage of the disease. The aim of [...] Read more.
Beyond sleep/wake, clock genes regulate the daily rhythms of melatonin production, motor activity, innate immunity, and mitochondrial dynamics, among others. All these rhythms are affected in Parkinson’s disease (PD), suggesting that chronodisruption may be an early stage of the disease. The aim of this study was to evaluate the connection between clock genes and these rhythms in PD, and whether melatonin administration reestablished the normal clock function. Parkinsonism was induced with 600 μM MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) in 24–120 h post fertilization (hpf) zebrafish embryos and melatonin was administered at a dose of 1 μM. Day–night melatonin rhythm disappeared in MPTP-treated embryos, which showed an advance in the activity phase in parallel with changes in the rhythm of clock genes. An alteration in the fission-to-fusion mitochondrial dynamics was also detected in parkinsonian embryos, increasing the former and leading to apoptosis. Melatonin administration to MPTP-treated embryos fully restored the circadian system, including the rhythms of clock genes, motor activity, melatonin rhythm, and mitochondrial dynamics, and decreasing apoptosis. Because clock-controlled rhythms such as sleep/wake alterations are early events in PD, the data here reported may point to chronodisruption as one initial pathophysiological event of the disease. Full article
(This article belongs to the Special Issue Natural Antioxidants in Neurodegeneration and Aging Processes)
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13 pages, 1695 KiB  
Article
Quercetin Nanoemulsion Ameliorates Neuronal Dysfunction in Experimental Alzheimer’s Disease Model
by Nouf K. Alaqeel, Mona H. AlSheikh and Mohammed T. Al-Hariri
Antioxidants 2022, 11(10), 1986; https://doi.org/10.3390/antiox11101986 - 05 Oct 2022
Cited by 12 | Viewed by 2307
Abstract
Aluminum is the most abundant metal that can get admission to the human through several means that include our food, drinking water, cans, drugs, and deodorants, causing neurodegenerative diseases such as Alzheimer’s disease (AD). The present study aims to evaluate the role of [...] Read more.
Aluminum is the most abundant metal that can get admission to the human through several means that include our food, drinking water, cans, drugs, and deodorants, causing neurodegenerative diseases such as Alzheimer’s disease (AD). The present study aims to evaluate the role of quercetin nanoemulsion (QCNE) in attenuating neuronal dysfunction in aluminum chloride (AlCl3)-induced experimental AD. All animals were classified into six groups including negative control group (I): received a vehicle; QC group: received intraperitoneal (IP) injection of QC; Alzheimer’s group: received AlCl3 orally; treated group (I): received AlCl3 orally and IP injection of QC; treated group (II): received AlCl3 orally and QC orally; and treated group (III): received AlCl3 orally and IP injection of QCNE. At the end of the experimental period (30 days), the brain was used to study biochemical parameters (measurement of neurotransmitters (serotonin, dopamine, and norepinephrine), oxidant/antioxidant parameters (reduced glutathione, malondialdehyde, superoxide dismutase, and advanced oxidation protein product), and inflammatory markers (adiponectin, interleukin 1β, and plasma tumor necrosis factor-alpha)), while another part was for brain immune-histochemical analysis (study cyclooxygenases (COX-1 and COX-2)). Results showed that the mean value of oxidative stress markers was significantly increased in the AD group as well as the inflammatory biomarkers and all the study neurotransmitters, whereas these parameters were attenuated in treated groups, especially those that received QCNE. The immunohistochemistry findings confirm our results. Both approaches (QC and QCNE) succeeded in retracting the negative impact of AlCl3. Meanwhile, the effect of QCNE is more potent in mitigating the impact mediated by AlCl3 in treated animals. In conclusion, the treatment mainly by QCNE has huge potential in protecting against AlCl3-induced neuronal dysfunction, as shown in our results by the elevation of brain antioxidant/anti-inflammatory activities and neurotransmitter levels as well as mending of the histopathological changes in animal models. Full article
(This article belongs to the Special Issue Natural Antioxidants in Neurodegeneration and Aging Processes)
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