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Antioxidant Therapies in Acute and Chronic Neurodegenerations
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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 8529

Special Issue Editors

Prof. Dr. Giuseppe Lazzarino

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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
Departmental Faculty of Medicine and Surgery, 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

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

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

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

Published Papers (3 papers)

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26 pages, 4022 KiB  
Article
Gene Expression Profile as a Predictor of Seizure Liability
by Anssi Lipponen, Natallie Kajevu, Teemu Natunen, Robert Ciszek, Noora Puhakka, Mikko Hiltunen and Asla Pitkänen
Int. J. Mol. Sci. 2023, 24(4), 4116; https://doi.org/10.3390/ijms24044116 - 18 Feb 2023
Viewed by 1622
Abstract
Analysis platforms to predict drug-induced seizure liability at an early phase of drug development would improve safety and reduce attrition and the high cost of drug development. We hypothesized that a drug-induced in vitro transcriptomics signature predicts its ictogenicity. We exposed rat cortical [...] Read more.
Analysis platforms to predict drug-induced seizure liability at an early phase of drug development would improve safety and reduce attrition and the high cost of drug development. We hypothesized that a drug-induced in vitro transcriptomics signature predicts its ictogenicity. We exposed rat cortical neuronal cultures to non-toxic concentrations of 34 compounds for 24 h; 11 were known to be ictogenic (tool compounds), 13 were associated with a high number of seizure-related adverse event reports in the clinical FDA Adverse Event Reporting System (FAERS) database and systematic literature search (FAERS-positive compounds), and 10 were known to be non-ictogenic (FAERS-negative compounds). The drug-induced gene expression profile was assessed from RNA-sequencing data. Transcriptomics profiles induced by the tool, FAERS-positive and FAERS-negative compounds, were compared using bioinformatics and machine learning. Of the 13 FAERS-positive compounds, 11 induced significant differential gene expression; 10 of the 11 showed an overall high similarity to the profile of at least one tool compound, correctly predicting the ictogenicity. Alikeness-% based on the number of the same differentially expressed genes correctly categorized 85%, the Gene Set Enrichment Analysis score correctly categorized 73%, and the machine-learning approach correctly categorized 91% of the FAERS-positive compounds with reported seizure liability currently in clinical use. Our data suggest that the drug-induced gene expression profile could be used as a predictive biomarker for seizure liability. Full article
(This article belongs to the Special Issue Antioxidant Therapies in Acute and Chronic Neurodegenerations)
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29 pages, 6663 KiB  
Article
Targeting Oxidative Stress with Antioxidant Duotherapy after Experimental Traumatic Brain Injury
by Jenni Kyyriäinen, Natallie Kajevu, Ivette Bañuelos, Leonardo Lara, Anssi Lipponen, Silvia Balosso, Elina Hämäläinen, Shalini Das Gupta, Noora Puhakka, Teemu Natunen, Teresa Ravizza, Annamaria Vezzani, Mikko Hiltunen and Asla Pitkänen
Int. J. Mol. Sci. 2021, 22(19), 10555; https://doi.org/10.3390/ijms221910555 - 29 Sep 2021
Cited by 5 | Viewed by 2578
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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24 pages, 4115 KiB  
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
by Olga O. Gonchar, Andriy V. Maznychenko, Olena M. Klyuchko, Iryna M. Mankovska, Kamila Butowska, Agnieszka Borowik, Jacek Piosik and Inna Sokolowska
Int. J. Mol. Sci. 2021, 22(11), 5444; https://doi.org/10.3390/ijms22115444 - 21 May 2021
Cited by 23 | Viewed by 3475
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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