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Special Issue "Antioxidant Therapies in Acute and Chronic Neurodegenerations"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 3658

Special Issue Editors

Prof. Dr. Giuseppe Lazzarino
E-Mail Website
Guest Editor
Department of Biomedical and Biotechnological Sciences (BIOMETEC), University of Catania, 95123 Catania, Italy
Interests: mitochondrial dysfunction; traumatic brain injury, oxidative/nitrosative stress; energy metabolism; neurodegenerations
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Barbara Tavazzi
E-Mail Website
Guest Editor
Full Professor of Biochemistry, Faculty Department - UniCamillus - Saint Camillus International University of Health and Medical Sciences, Via di Sant'Alessandro 8, 00131 Rome, Italy
Interests: neurodegenerative acute (traumatic brain injury) and chronic (multiple sclerosis) disorders; oxidative and nitrosative stresses; oxidation mechanisms; antioxidants; metabolomics; biochemical analytical techniques; lipid peroxidation products; dietary antioxidants; carotenoids; polyphenols; vitamin E; vitamin C; antioxidant activity/capacity
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Giacomo Lazzarino
E-Mail Website
Guest Editor
UniCamillus—Saint Camillus International University of Health Sciences, Via di Sant’Alessandro 8, 00131 Rome, Italy
Interests: mitochondrial dysfunction; oxidative/nitrosative stress; neurodegenerations; multiple sclerosis; traumatic brain injury; metabolic cell reprogramming
Special Issues, Collections and Topics in MDPI journals
Dr. Giuseppe Caruso
E-Mail Website
Guest Editor
Department of Drug and Health Sciences, University of Catania, 95125 Catania, Italy
Interests: carnosine; microglia/macrophages; inflammation; oxidative stress; Alzheimer’s disease; transforming growth factor-beta 1 (TGF-β1); neurodegeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acute (cerebral ischemia, traumatic brain injury) and chronic neurodegenerations (Alzheimer’s disease, Parkinson disease, amyotrophic lateral sclerosis, multiple sclerosis, Huntington disease), although caused by substantially different mechanisms, have some molecular features in common, including sustained oxidative/nitrosative stress, decreased antioxidant defenses, mitochondrial dysfunction with energy penalty, and neuroinflammation. Molecular and clinical damages in acute neurodegenerations are not necessarily progressive, although repeated episodes of acute neurodegenerations, of even mild severity, may evolve into chronic neurodegenerations, as occurs in repeated sports-related concussions potentially evolving into chronic traumatic encephalopathy (CTE). Differently, damages caused by chronic neurodegenerations progress at molecular level and are mirrored by worsening of patient clinical conditions (loss of cognitive and/or psychomotor functions). In the last decade, great attention has been given to the possibility of reducing the damaging effects produced by sustained oxidative/nitrosative stress as a key (and common) phenomenon involved in the molecular damages caused by acute and chronic neurodegenerations. Therefore, testing the effects of antioxidant administration to limit the damages of acute head injuries and to counteract progression of chronic neurodegenerations appears to be a therapeutic approach of great potential clinical utility.

This Special Issue is dedicated to preclinical and clinical studies significantly updating our knowledge on antioxidant therapies in acute and chronic neurodegenerations. Original articles should not simply be a phenomenological presentation of the data but should contain mechanistic indications on the eventual benefits produced by the antioxidant(s) in the selected pathology. Review articles are also welcome but they should contain an evaluation of the molecular aspects of the antioxidant-based therapies to date tested.

Prof. Dr. Giuseppe Lazzarino
Prof. Dr. Barbara Tavazzi
Prof. Dr. Giacomo Lazzarino
Dr. Giuseppe Caruso
Guest Editors

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • acute and chronic neurodegenerations
  • oxidative/nitrosative stress
  • antioxidants
  • mitochondrial dysfunction
  • neuroinflammation

Published Papers (2 papers)

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Research

Article
Targeting Oxidative Stress with Antioxidant Duotherapy after Experimental Traumatic Brain Injury
Int. J. Mol. Sci. 2021, 22(19), 10555; https://doi.org/10.3390/ijms221910555 - 29 Sep 2021
Cited by 2 | Viewed by 1331
Abstract
We assessed the effect of antioxidant therapy using the Food and Drug Administration-approved respiratory drug N-acetylcysteine (NAC) or sulforaphane (SFN) as monotherapies or duotherapy in vitro in neuron-BV2 microglial co-cultures and validated the results in a lateral fluid-percussion model of TBI in [...] Read more.
We assessed the effect of antioxidant therapy using the Food and Drug Administration-approved respiratory drug N-acetylcysteine (NAC) or sulforaphane (SFN) as monotherapies or duotherapy in vitro in neuron-BV2 microglial co-cultures and validated the results in a lateral fluid-percussion model of TBI in rats. As in vitro measures, we assessed neuronal viability by microtubule-associated-protein 2 immunostaining, neuroinflammation by monitoring tumor necrosis factor (TNF) levels, and neurotoxicity by measuring nitrite levels. In vitro, duotherapy with NAC and SFN reduced nitrite levels to 40% (p < 0.001) and neuroinflammation to –29% (p < 0.001) compared with untreated culture. The treatment also improved neuronal viability up to 72% of that in a positive control (p < 0.001). The effect of NAC was negligible, however, compared with SFN. In vivo, antioxidant duotherapy slightly improved performance in the beam walking test. Interestingly, duotherapy treatment decreased the plasma interleukin-6 and TNF levels in sham-operated controls (p < 0.05). After TBI, no treatment effect on HMGB1 or plasma cytokine levels was detected. Also, no treatment effects on the composite neuroscore or cortical lesion area were detected. The robust favorable effect of duotherapy on neuroprotection, neuroinflammation, and oxidative stress in neuron-BV2 microglial co-cultures translated to modest favorable in vivo effects in a severe TBI model. Full article
(This article belongs to the Special Issue Antioxidant Therapies in Acute and Chronic Neurodegenerations)
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Article
C60 Fullerene Reduces 3-Nitropropionic Acid-Induced Oxidative Stress Disorders and Mitochondrial Dysfunction in Rats by Modulation of p53, Bcl-2 and Nrf2 Targeted Proteins
Int. J. Mol. Sci. 2021, 22(11), 5444; https://doi.org/10.3390/ijms22115444 - 21 May 2021
Cited by 9 | Viewed by 1785
Abstract
C60 fullerene as a potent free radical scavenger and antioxidant could be a beneficial means for neurodegenerative disease prevention or cure. The aim of the study was to define the effects of C60 administration on mitochondrial dysfunction and oxidative stress disorders [...] Read more.
C60 fullerene as a potent free radical scavenger and antioxidant could be a beneficial means for neurodegenerative disease prevention or cure. The aim of the study was to define the effects of C60 administration on mitochondrial dysfunction and oxidative stress disorders in a 3-nitropropionic acid (3-NPA)-induced rat model of Huntington’s disease. Animals received 3-NPA (30 mg/kg i.p.) once a day for 3 consecutive days. C60 was applied at a dose of 0.5 mg/kg of body weight, i.p. daily over 5 days before (C60 pre-treatment) and after 3-NPA exposure (C60 post-treatment). Oxidative stress biomarkers, the activity of respiratory chain enzymes, the level of antioxidant defense, and pro- and antiapoptotic markers were analyzed in the brain and skeletal muscle mitochondria. The nuclear and cytosol Nrf2 protein expression, protein level of MnSOD, γ-glutamate-cysteine ligase (γ-GCLC), and glutathione-S-transferase (GSTP) as Nrf2 targets were evaluated. Our results indicated that C60 can prevent 3-NPA-induced mitochondrial dysfunction through the restoring of mitochondrial complexes’ enzyme activity, ROS scavenging, modulating of pro/antioxidant balance and GSH/GSSG ratio, as well as inhibition of mitochondria-dependent apoptosis through the limitation of p53 mitochondrial translocation and increase in Bcl-2 protein expression. C60 improved mitochondrial protection by strengthening the endogenous glutathione system via glutathione biosynthesis by up-regulating Nrf2 nuclear accumulation as well as GCLC and GSTP protein level. Full article
(This article belongs to the Special Issue Antioxidant Therapies in Acute and Chronic Neurodegenerations)
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