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Antioxidants
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Antioxidant Capability and Physical Exercise in Neurobiology: A Focus in...
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Antioxidant Capability and Physical Exercise in Neurobiology: A Focus in Neurodegeneration

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

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 27123

Special Issue Editor

Dr. Ferdinando Franzoni

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy
Interests: oxidative stress; brain function; neurodegeneration; antioxidant capability; physical exercise
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative processes have been linked not only to genetic factors but also to environmental ones. Among these, a pivotal role has been largely attributed to oxidative stress, which arises from an imbalance between an excessive generation of reactive oxygen species (ROS) and the biological system’s capability to eliminate the reactive intermediates. Oxidative stress leads to a progressive decline in cell physiology by damaging cellular macromolecular components such as DNA, lipids, and proteins.

Several studies have demonstrated that regular exercise is an important preventive and therapeutic tool in neurodegeneration and cerebrovascular diseases. The adaptive response to regular exercise involves the upregulation of the enzymatic antioxidant system and modulation of oxidative damage, which culminate in a recovered redox state of brain cells. In addition to a reduction in oxidative damage, the effects of exercise seem to be quite intricate, including an increase in neurogenesis and capillarization and an enhanced proteolytic degradation of toxic oligomers that characterize aging and neurodegenerative processes. All together, these data highlight the link between neurodegeneration, oxidative stress, and physical exercise.

This Special Issue aims to provide an overview of the current knowledge on the physiological, metabolic, and epigenetic modifications in response to physical activity and its final effects on brain functionality, both in physiological and in pathological conditions.

Potential topics include, but are not limited to, the following:

Studies of the cellular and molecular mechanisms associated with oxidative stress in neurodegenerative diseases;

Clinical or preclinical studies showing physical exercise properties in brain functionality.

Prof. Ferdinando Franzoni
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

  • Physical exercise
  • Oxidative stress
  • Brain function
  • Neurodegeneration
  • Antioxidant capability

Related Special Issue

Published Papers (5 papers)

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Editorial

Jump to: Research, Review

2 pages, 166 KiB  
Editorial
Antioxidant Capability and Physical Exercise in Neurobiology: A Focus in Neurodegeneration
by Giorgia Scarfò, Simona Daniele and Ferdinando Franzoni
Antioxidants 2021, 10(2), 250; https://doi.org/10.3390/antiox10020250 - 6 Feb 2021
Cited by 1 | Viewed by 1820
Abstract
Neurodegeneration is a complex process controlled by both genetic and environmental factors [...] Full article
(This article belongs to the Special Issue Antioxidant Capability and Physical Exercise in Neurobiology: A Focus in Neurodegeneration)

Research

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16 pages, 1171 KiB  
Article
Co-Administration of Iron and a Bioavailable Curcumin Supplement Increases Serum BDNF Levels in Healthy Adults
by Helena Tiekou Lorinczova, Owen Fitzsimons, Leah Mursaleen, Derek Renshaw, Gulshanara Begum and Mohammed Gulrez Zariwala
Antioxidants 2020, 9(8), 645; https://doi.org/10.3390/antiox9080645 - 22 Jul 2020
Cited by 16 | Viewed by 9477
Abstract
Brain-derived neurotrophic factor (BDNF) is key for the maintenance of normal neuronal function and energy homeostasis and has been suggested to improve cognitive function, including learning and memory. Iron and the antioxidant curcumin have been shown to influence BDNF homeostasis. This 6-week, double [...] Read more.
Brain-derived neurotrophic factor (BDNF) is key for the maintenance of normal neuronal function and energy homeostasis and has been suggested to improve cognitive function, including learning and memory. Iron and the antioxidant curcumin have been shown to influence BDNF homeostasis. This 6-week, double blind, randomized, placebo-controlled study examined the effects of oral iron supplementation at low (18 mg) and high (65 mg) ferrous (FS) iron dosages, compared to a combination of these iron doses with a bioavailable formulated form of curcumin (HydroCurcTM; 500 mg) on BDNF levels in a healthy adult cohort of 155 male (26.42 years ± 0.55) and female (25.82 years ± 0.54) participants. Participants were randomly allocated to five different treatment groups: both iron and curcumin placebo (FS0+Plac), low dose iron and curcumin placebo (FS18+Plac), low dose iron and curcumin (FS18+Curc), high dose iron and curcumin placebo (FS65+Plac) and high dose iron and curcumin (FS65+Curc). Results showed a significant increase in BDNF over time (26%) in the FS18+Curc group (p = 0.024), and at end-point between FS18+Curc and FS18+Plac groups (35%, p = 0.042), demonstrating for the first time that the combination with curcumin, rather than iron supplementation alone, results in increased serum BDNF. The addition of curcumin to iron supplementation may therefore provide a novel approach to further enhance the benefits associated with increased BDNF levels. Full article
(This article belongs to the Special Issue Antioxidant Capability and Physical Exercise in Neurobiology: A Focus in Neurodegeneration)
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21 pages, 3733 KiB  
Article
N-Acetylcysteine Nanocarriers Protect against Oxidative Stress in a Cellular Model of Parkinson’s Disease
by Leah Mursaleen, Brendon Noble, Stefanie Ho Yi Chan, Satyanarayana Somavarapu and Mohammed Gulrez Zariwala
Antioxidants 2020, 9(7), 600; https://doi.org/10.3390/antiox9070600 - 9 Jul 2020
Cited by 27 | Viewed by 4753
Abstract
Oxidative stress is a key mediator in the development and progression of Parkinson’s disease (PD). The antioxidant N-acetylcysteine (NAC) has generated interest as a disease-modifying therapy for PD but is limited due to poor bioavailability, a short half-life, and limited access to [...] Read more.
Oxidative stress is a key mediator in the development and progression of Parkinson’s disease (PD). The antioxidant N-acetylcysteine (NAC) has generated interest as a disease-modifying therapy for PD but is limited due to poor bioavailability, a short half-life, and limited access to the brain. The aim of this study was to formulate and utilise mitochondria-targeted nanocarriers for delivery of NAC alone and in combination with the iron chelator deferoxamine (DFO), and assess their ability to protect against oxidative stress in a cellular rotenone PD model. Pluronic F68 (P68) and dequalinium (DQA) nanocarriers were prepared by a modified thin-film hydration method. An MTT assay assessed cell viability and iron status was measured using a ferrozine assay and ferritin immunoassay. For oxidative stress, a modified cellular antioxidant activity assay and the thiobarbituric acid-reactive substances assay and mitochondrial hydroxyl assay were utilised. Overall, this study demonstrates, for the first time, successful formulation of NAC and NAC + DFO into P68 + DQA nanocarriers for neuronal delivery. The results indicate that NAC and NAC + DFO nanocarriers have the potential characteristics to access the brain and that 1000 μM P68 + DQA NAC exhibited the strongest ability to protect against reduced cell viability (p = 0.0001), increased iron (p = 0.0033) and oxidative stress (p ≤ 0.0003). These NAC nanocarriers therefore demonstrate significant potential to be transitioned for further preclinical testing for PD. Full article
(This article belongs to the Special Issue Antioxidant Capability and Physical Exercise in Neurobiology: A Focus in Neurodegeneration)
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24 pages, 6148 KiB  
Article
The Impact of Acetyl-CoA and Aspartate Shortages on the N-Acetylaspartate Level in Different Models of Cholinergic Neurons
by Marlena Zyśk, Monika Sakowicz-Burkiewicz, Piotr Pikul, Robert Kowalski, Anna Michno and Tadeusz Pawełczyk
Antioxidants 2020, 9(6), 522; https://doi.org/10.3390/antiox9060522 - 13 Jun 2020
Cited by 8 | Viewed by 3689
Abstract
N-acetylaspartate is produced by neuronal aspartate N-acetyltransferase (NAT8L) from acetyl-CoA and aspartate. In cholinergic neurons, acetyl-CoA is also utilized in the mitochondrial tricarboxylic acid cycle and in acetylcholine production pathways. While aspartate has to be shared with the malate–aspartate shuttle, another mitochondrial [...] Read more.
N-acetylaspartate is produced by neuronal aspartate N-acetyltransferase (NAT8L) from acetyl-CoA and aspartate. In cholinergic neurons, acetyl-CoA is also utilized in the mitochondrial tricarboxylic acid cycle and in acetylcholine production pathways. While aspartate has to be shared with the malate–aspartate shuttle, another mitochondrial machinery together with the tricarboxylic acid cycle supports the electron transport chain turnover. The main goal of this study was to establish the impact of toxic conditions on N-acetylaspartate production. SN56 cholinergic cells were exposed to either Zn2+ overload or Ca2+ homeostasis dysregulation and male adult Wistar rats’ brains were studied after 2 weeks of challenge with streptozotocin-induced hyperglycemia or daily theophylline treatment. Our results allow us to hypothesize that the cholinergic neurons from brain septum prioritized the acetylcholine over N-acetylaspartate production. This report provides the first direct evidence for Zn2+-dependent suppression of N-acetylaspartate synthesis leading to mitochondrial acetyl-CoA and aspartate shortages. Furthermore, Zn2+ is a direct concentration-dependent inhibitor of NAT8L activity, while Zn2+-triggered oxidative stress is unlikely to be significant in such suppression. Full article
(This article belongs to the Special Issue Antioxidant Capability and Physical Exercise in Neurobiology: A Focus in Neurodegeneration)
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Review

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12 pages, 1060 KiB  
Review
Aerobic Exercise and Healthy Nutrition as Neuroprotective Agents for Brain Health in Patients with Parkinson’s Disease: A Critical Review of the Literature
by Davide Maria Cammisuli, Ubaldo Bonuccelli, Simona Daniele, Claudia Martini, Jonathan Fusi and Ferdinando Franzoni
Antioxidants 2020, 9(5), 380; https://doi.org/10.3390/antiox9050380 - 5 May 2020
Cited by 13 | Viewed by 6661
Abstract
Parkinson’s disease (PD) is characterized by motor and nonmotor features that have an influence on patients’ quality of life at different levels. To date, some evidences have arisen on the effectiveness of physical trainings and nutrients intake in ameliorating functional and cognitive outcomes [...] Read more.
Parkinson’s disease (PD) is characterized by motor and nonmotor features that have an influence on patients’ quality of life at different levels. To date, some evidences have arisen on the effectiveness of physical trainings and nutrients intake in ameliorating functional and cognitive outcomes in PD patients. Physical activity is effective in improving both motor and nonmotor features and recent epidemiological investigations have revealed the pivotal role that dietary patterns may play in reducing the risk of PD highlighting the pathogenesis of the neurodegeneration. Specifically, aerobic exercise shows beneficial effects in improving motor functions and executive control in PD patients, as well as proper nutrition may help in improving neuroprotective agents counteracting neurodegeneration and allows patients to better interact with the medication. Our narrative review critically focused on aerobic exercise and nutrition in PD in order to point out the best prescriptions for brain health of affected patients. Implications for a therapeutic plan and rehabilitation for these patients are also discussed. Full article
(This article belongs to the Special Issue Antioxidant Capability and Physical Exercise in Neurobiology: A Focus in Neurodegeneration)
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