Special Issue "Antioxidant and Neuroprotection"

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (31 July 2017)

Special Issue Editors

Guest Editor
Dr. David Vauzour

Department of Nutrition, Norwich Medical School, Faculty of Medicine and Health Sciences, University of East Anglia, Norwich NR4 7TJ, UK
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Interests: neurodegenerative disorders; phytochemicals; neuroinflammation; memory; learning and neuro-cognitive performances; signalling pathways; oxidative stress
Guest Editor
Prof. Dr. Rita Businaro

Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Italy
Website | E-Mail

Special Issue Information

Dear Colleagues,

As people age, their cognitive functions are threatened by the normal ageing process, as well as an increasing risk for neurodegenerative conditions. Although the exact causes underlying those behavioral and neuronal declines have not been fully elucidated, recent evidence suggests that antioxidants may exert neuroprotective actions through the potential to protect neurons against neurotoxin-induced injury, neuroinflammation, and the potential to promote memory, learning, and cognitive performance. However, despite significant advances in our understanding of the biology of these molecules, the exact molecular and cellular mechanisms underlying their biological effects are still unclear. It is nonetheless evident that such nutrients are potent bioactive molecules, and a clear understanding of their precise mechanisms of action, as either antioxidants or modulators of cell signalling, is crucial for the evaluation of their potential as neuroprotective agents.

We invite investigators to contribute full length original research articles, as well as review articles, that will stimulate the continuing efforts in understand the precise effects of antioxidant compounds in vitro and in vivo. We are particularly interested in articles describing the molecular mechanisms of action by which these molecules exert their modulatory effects in neurodegenerative diseases.

Dr. David Vauzour
Prof. Dr. Rita Businaro
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 papers will be 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 550 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

  • Antioxidants;
  • Cell signalling;
  • Neurons;
  • Astrocytes;
  • Microglia;
  • Cognitive decline;
  • Neuroprotection;
  • Ageing

Published Papers (6 papers)

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Research

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Open AccessArticle Procyanidin B2 Protects Neurons from Oxidative, Nitrosative, and Excitotoxic Stress
Antioxidants 2017, 6(4), 77; https://doi.org/10.3390/antiox6040077
Received: 29 July 2017 / Revised: 23 September 2017 / Accepted: 5 October 2017 / Published: 13 October 2017
Cited by 2 | PDF Full-text (8379 KB) | HTML Full-text | XML Full-text
Abstract
The aberrant generation of oxygen and nitrogen free radicals can cause severe damage to key cellular components, resulting in cell apoptosis. Similarly, excitotoxicity leads to protease activation and mitochondrial dysfunction, which subsequently causes cell death. Each of these factors play critical roles in
[...] Read more.
The aberrant generation of oxygen and nitrogen free radicals can cause severe damage to key cellular components, resulting in cell apoptosis. Similarly, excitotoxicity leads to protease activation and mitochondrial dysfunction, which subsequently causes cell death. Each of these factors play critical roles in the neuronal cell death underlying various neurodegenerative diseases. Procyanidin B2 (PB2) is a naturally occurring polyphenolic compound found in high concentrations in cocoa, apples, and grapes. Here, we examine the neuroprotective effects of PB2 in primary cultures of rat cerebellar granule neurons (CGNs) exposed to various stressors. CGNs were pre-incubated with PB2 and then neuronal stress was induced as described below. Mitochondrial oxidative stress was triggered with HA14-1, an inhibitor of the pro-survival Bcl-2 protein which induces glutathione-sensitive apoptosis. Glutamate and glycine were used to induce excitotoxicity. Sodium nitroprusside, a nitric oxide generating compound, was used to induce nitrosative stress. We observed significant dose-dependent protection of CGNs with PB2 for all of the above insults, with the greatest neuroprotective effect being observed under conditions of nitrosative stress. Intriguingly, the neuroprotective effect of PB2 against nitric oxide was superoxide-dependent, as we have recently shown for other catechol antioxidants. Finally, we induced neuronal stress through the removal of depolarizing extracellular potassium and serum (5K conditions), which is a classical model of intrinsic apoptosis in CGNs. PB2 did not display any significant protection against 5K-induced apoptosis at any concentration tested. We conclude that PB2 offers neuronal protection principally as an antioxidant by scavenging reactive oxygen and nitrogen species instead of through modulation of pro-survival cell signaling pathways. These findings suggest that PB2 may be an effective neuroprotective agent for the treatment of neurodegenerative disorders. Full article
(This article belongs to the Special Issue Antioxidant and Neuroprotection)
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Open AccessArticle S-Adenosylmethionine and Superoxide Dismutase 1 Synergistically Counteract Alzheimer’s Disease Features Progression in TgCRND8 Mice
Antioxidants 2017, 6(4), 76; https://doi.org/10.3390/antiox6040076
Received: 26 July 2017 / Revised: 26 September 2017 / Accepted: 27 September 2017 / Published: 30 September 2017
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Abstract
Recent evidence emphasizes the role of dysregulated one-carbon metabolism in Alzheimer’s Disease (AD). Exploiting a nutritional B-vitamin deficiency paradigm, we have previously shown that PSEN1 and BACE1 activity is modulated by one-carbon metabolism, leading to increased amyloid production. We have also demonstrated that
[...] Read more.
Recent evidence emphasizes the role of dysregulated one-carbon metabolism in Alzheimer’s Disease (AD). Exploiting a nutritional B-vitamin deficiency paradigm, we have previously shown that PSEN1 and BACE1 activity is modulated by one-carbon metabolism, leading to increased amyloid production. We have also demonstrated that S-adenosylmethionine (SAM) supplementation contrasted the AD-like features, induced by B-vitamin deficiency. In the present study, we expanded these observations by investigating the effects of SAM and SOD (Superoxide dismutase) association. TgCRND8 AD mice were fed either with a control or B-vitamin deficient diet, with or without oral supplementation of SAM + SOD. We measured oxidative stress by lipid peroxidation assay, PSEN1 and BACE1 expression by Real-Time Polymerase Chain Reaction (PCR), amyloid deposition by ELISA assays and immunohistochemistry. We found that SAM + SOD supplementation prevents the exacerbation of AD-like features induced by B vitamin deficiency, showing synergistic effects compared to either SAM or SOD alone. SAM + SOD supplementation also contrasts the amyloid deposition typically observed in TgCRND8 mice. Although the mechanisms underlying the beneficial effect of exogenous SOD remain to be elucidated, our findings identify that the combination of SAM + SOD could be carefully considered as co-adjuvant of current AD therapies. Full article
(This article belongs to the Special Issue Antioxidant and Neuroprotection)
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Open AccessCommunication Alpha-Lipoic Acid Downregulates IL-1β and IL-6 by DNA Hypermethylation in SK-N-BE Neuroblastoma Cells
Antioxidants 2017, 6(4), 74; https://doi.org/10.3390/antiox6040074
Received: 26 July 2017 / Revised: 18 September 2017 / Accepted: 23 September 2017 / Published: 26 September 2017
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Abstract
Alpha-lipoic acid (ALA) is a pleiotropic molecule with antioxidant and anti-inflammatory properties, of which the effects are exerted through the modulation of NF-kB. This nuclear factor, in fact, modulates different inflammatory cytokines, including IL-1b and IL-6, in different tissues and cell types. We
[...] Read more.
Alpha-lipoic acid (ALA) is a pleiotropic molecule with antioxidant and anti-inflammatory properties, of which the effects are exerted through the modulation of NF-kB. This nuclear factor, in fact, modulates different inflammatory cytokines, including IL-1b and IL-6, in different tissues and cell types. We recently showed that IL-1b and IL-6 DNA methylation is modulated in the brain of Alzheimer’s disease patients, and that IL-1b expression is associated to DNA methylation in the brain of patients with tuberous sclerosis complex. These results prompted us to ask whether ALA-induced repression of IL-1b and IL-6 was dependent on DNA methylation. Therefore, we profiled DNA methylation in the 5’-flanking region of the two aforementioned genes in SK-N-BE human neuroblastoma cells cultured in presence of ALA 0.5 mM. Our experimental data pointed out that the two promoters are hypermethylated in cells supplemented with ALA, both at CpG and non-CpG sites. Moreover, the observed hypermethylation is associated with decreased mRNA expression and decreased cytokine release. These results reinforce previous findings indicating that IL-1b and IL-6 undergo DNA methylation-dependent modulation in neural models and pave the road to study the epigenetic mechanisms triggered by ALA. Full article
(This article belongs to the Special Issue Antioxidant and Neuroprotection)
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Review

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Open AccessReview Anti-Oxidant and Anti-Inflammatory Activity of Ketogenic Diet: New Perspectives for Neuroprotection in Alzheimer’s Disease
Antioxidants 2018, 7(5), 63; https://doi.org/10.3390/antiox7050063
Received: 30 March 2018 / Revised: 23 April 2018 / Accepted: 25 April 2018 / Published: 28 April 2018
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Abstract
The ketogenic diet, originally developed for the treatment of epilepsy in non-responder children, is spreading to be used in the treatment of many diseases, including Alzheimer’s disease. The main activity of the ketogenic diet has been related to improved mitochondrial function and decreased
[...] Read more.
The ketogenic diet, originally developed for the treatment of epilepsy in non-responder children, is spreading to be used in the treatment of many diseases, including Alzheimer’s disease. The main activity of the ketogenic diet has been related to improved mitochondrial function and decreased oxidative stress. B-Hydroxybutyrate, the most studied ketone body, has been shown to reduce the production of reactive oxygen species (ROS), improving mitochondrial respiration: it stimulates the cellular endogenous antioxidant system with the activation of nuclear factor erythroid-derived 2-related factor 2 (Nrf2), it modulates the ratio between the oxidized and reduced forms of nicotinamide adenine dinucleotide (NAD+/NADH) and it increases the efficiency of electron transport chain through the expression of uncoupling proteins. Furthermore, the ketogenic diet performs anti-inflammatory activity by inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) activation and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome as well as inhibiting histone deacetylases (HDACs), improving memory encoding. The underlying mechanisms and the perspectives for the treatment of Alzheimer’s disease are discussed. Full article
(This article belongs to the Special Issue Antioxidant and Neuroprotection)
Open AccessReview Modulation of Nrf2 by Olive Oil and Wine Polyphenols and Neuroprotection
Antioxidants 2017, 6(4), 73; https://doi.org/10.3390/antiox6040073
Received: 31 July 2017 / Revised: 19 September 2017 / Accepted: 20 September 2017 / Published: 26 September 2017
Cited by 2 | PDF Full-text (651 KB) | HTML Full-text | XML Full-text
Abstract
Strong adherence to a Mediterranean diet is associated with improved cognitive function and a lower prevalence of mild cognitive impairment. Olive oil and red wine are rich sources of polyphenols which are responsible in part for the beneficial effects on cognitive functioning. Polyphenols
[...] Read more.
Strong adherence to a Mediterranean diet is associated with improved cognitive function and a lower prevalence of mild cognitive impairment. Olive oil and red wine are rich sources of polyphenols which are responsible in part for the beneficial effects on cognitive functioning. Polyphenols induce endogenous antioxidant defense mechanisms by modulating transcription factors such as the nuclear factor (erythroid-derived 2)-like 2 (Nrf2). This review discusses the scientific data supporting the modulating effect of olive oil and red wine polyphenols on Nrf2 expression, and the potential health benefits associated with cognitive functioning. Full article
(This article belongs to the Special Issue Antioxidant and Neuroprotection)
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Open AccessReview Molecular Mechanisms behind Free Radical Scavengers Function against Oxidative Stress
Antioxidants 2017, 6(3), 51; https://doi.org/10.3390/antiox6030051
Received: 27 May 2017 / Revised: 26 June 2017 / Accepted: 29 June 2017 / Published: 10 July 2017
Cited by 5 | PDF Full-text (265 KB) | HTML Full-text | XML Full-text
Abstract
Accumulating evidence shows that oxidative stress is involved in a wide variety of human diseases: rheumatoid arthritis, Alzheimer’s disease, Parkinson’s disease, cancers, etc. Here, we discuss the significance of oxidative conditions in different disease, with the focus on neurodegenerative disease including Parkinson’s disease,
[...] Read more.
Accumulating evidence shows that oxidative stress is involved in a wide variety of human diseases: rheumatoid arthritis, Alzheimer’s disease, Parkinson’s disease, cancers, etc. Here, we discuss the significance of oxidative conditions in different disease, with the focus on neurodegenerative disease including Parkinson’s disease, which is mainly caused by oxidative stress. Reactive oxygen and nitrogen species (ROS and RNS, respectively), collectively known as RONS, are produced by cellular enzymes such as myeloperoxidase, NADPH-oxidase (nicotinamide adenine dinucleotide phosphate-oxidase) and nitric oxide synthase (NOS). Natural antioxidant systems are categorized into enzymatic and non-enzymatic antioxidant groups. The former includes a number of enzymes such as catalase and glutathione peroxidase, while the latter contains a number of antioxidants acquired from dietary sources including vitamin C, carotenoids, flavonoids and polyphenols. There are also scavengers used for therapeutic purposes, such as 3,4-dihydroxyphenylalanine (L-DOPA) used routinely in the treatment of Parkinson’s disease (not as a free radical scavenger), and 3-methyl-1-phenyl-2-pyrazolin-5-one (Edaravone) that acts as a free radical detoxifier frequently used in acute ischemic stroke. The cell surviving properties of L-DOPA and Edaravone against oxidative stress conditions rely on the alteration of a number of stress proteins such as Annexin A1, Peroxiredoxin-6 and PARK7/DJ-1 (Parkinson disease protein 7, also known as Protein deglycase DJ-1). Although they share the targets in reversing the cytotoxic effects of H2O2, they seem to have distinct mechanism of function. Exposure to L-DOPA may result in hypoxia condition and further induction of ORP150 (150-kDa oxygen-regulated protein) with its concomitant cytoprotective effects but Edaravone seems to protect cells via direct induction of Peroxiredoxin-2 and inhibition of apoptosis. Full article
(This article belongs to the Special Issue Antioxidant and Neuroprotection)
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