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Antioxidants
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Antioxidants and Anti-inflammatory Effects in Neurodegenerative Diseases
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Antioxidants and Anti-inflammatory Effects in Neurodegenerative Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 33829

Special Issue Editors

Prof. Dr. Irene Paterniti

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Guest Editor
Dipartimento di Medicina Clinica e Sperimentale, Università degli Studi di Messina, Messina, Italy
Interests: cancer; neuro-oncology; neurodegenerative diseases; pharmacology; inflammation; apoptosis
Special Issues, Collections and Topics in MDPI journals
Dr. Michela Campolo

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D’Alcontres, 31-98166 Messina, Italy
Interests: neurodegeneration; neuroinflammation; oxidative stress; CNS trauma; cell death
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Neurodegenerative diseases represent debilitating conditions characterized by the degeneration of neuronal cells in specific areas of the brain. Oxidative stress and inflammation are the hallmark of neurodegenerative disorders, contributing to the pathogenesis of progressive neurodegenerative syndromes, such as Alzheimer's disease and Parkinson's disease, as well as acute syndromes of neurodegeneration, such as ischaemic and haemorrhagic stroke. New research has identified several basic mechanisms that drive neurodegeneration triggered by inflammatory cells and their mediators at various stages of the neurodegenerative cascade. Knowing the role of oxidative stress and inflammation processes in neurodegeneration, the use of molecules with antioxidant and anti-inflammatory activities could represent a possible strategy for the treatment of neurodegenerative diseases and a promising approach to slowing the progression and limiting the extent of neuronal cell loss in these disorders. This Special Issue aims to collect papers considering all aspects of oxidative stress and inflammation in neurodegenerative diseases, highlighting the potential properties of antioxidative and anti-inflammatory molecules and their signaling to offer a complete understanding of these diseases. Articles describing recent discoveries in the field of neurodegenerative diseases, with particular attention to the involvement of neuronal oxidative stress and anti-inflammation, are especially welcome.

Dr. Irene Paterniti
Dr. Michela Campolo
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

  • Alzheimer’s disease
  • Parkinson’s disease
  • Multiple sclerosis
  • Huntington's disease
  • Neuroinflammation
  • Astrogliosis
  • Microgliosis
  • Oxidative stress
  • Apoptosis
  • Autophagy

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Published Papers (7 papers)

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Editorial

Jump to: Research, Review

2 pages, 179 KiB  
Editorial
Antioxidants and Anti-Inflammatory Effects in Neurodegenerative Diseases (NDs)
by Michela Campolo and Irene Paterniti
Antioxidants 2022, 11(6), 1172; https://doi.org/10.3390/antiox11061172 - 14 Jun 2022
Cited by 1 | Viewed by 1816
Abstract
Neurodegenerative diseases (NDs) are the most common chronic neurological diseases associated with age, and they have a strong impact on the patient’s quality of life [...] Full article
(This article belongs to the Special Issue Antioxidants and Anti-inflammatory Effects in Neurodegenerative Diseases)
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Research

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28 pages, 5284 KiB  
Article
Identification of Regulatory Factors and Prognostic Markers in Amyotrophic Lateral Sclerosis
by Hualin Sun, Ming Li, Yanan Ji, Jianwei Zhu, Zehao Chen, Lilei Zhang, Chunyan Deng, Qiong Cheng, Wei Wang, Yuntian Shen and Dingding Shen
Antioxidants 2022, 11(2), 303; https://doi.org/10.3390/antiox11020303 - 1 Feb 2022
Cited by 15 | Viewed by 3891
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive degeneration of motor neurons, leading to muscle atrophy, paralysis and even death. Immune disorder, redox imbalance, autophagy disorder, and iron homeostasis disorder have been shown to play critical roles in [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive degeneration of motor neurons, leading to muscle atrophy, paralysis and even death. Immune disorder, redox imbalance, autophagy disorder, and iron homeostasis disorder have been shown to play critical roles in the pathogenesis of ALS. However, the exact pathogenic genes and the underlying mechanism of ALS remain unclear. The purpose of this study was to screen for pathogenic regulatory genes and prognostic markers in ALS using bioinformatics methods. We used Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, gene set enrichment analysis (GSEA), and expression regulation network analysis to investigate the function of differentially expressed genes in the nerve tissue, lymphoid tissue, and whole blood of patients with ALS. Our results showed that the up-regulated genes were mainly involved in immune regulation and inflammation, and the down-regulated genes were mainly involved in energy metabolism and redox processes. Eleven up-regulated transcription factors (CEBPB, CEBPD, STAT5A, STAT6, RUNX1, REL, SMAD3, GABPB2, FOXO1, PAX6, and FOXJ1) and one down-regulated transcription factor (NOG) in the nerve tissue of patients with ALS likely play important regulatory roles in the pathogenesis of ALS. Based on construction and evaluation of the ALS biomarker screening model, cluster analysis of the identified characteristic genes, univariate Cox proportional hazards regression analysis, and the random survival forest algorithm, we found that MAEA, TPST1, IFNGR2, and ALAS2 may be prognostic markers regarding the survival of ALS patients. High expression of MAEA, TPST1, and IFNGR2 and low expression of ALAS2 in ALS patients may be closely related to short survival of ALS patients. Taken together, our results indicate that immune disorders, inflammation, energy metabolism, and redox imbalance may be the important pathogenic factors of ALS. CEBPB, CEBPD, STAT5A, STAT6, RUNX1, REL, SMAD3, GABPB2, FOXO1, PAX6, FOXJ1, and NOG may be important regulatory factors linked to the pathogenesis of ALS. MAEA, TPST1, IFNGR2, and ALAS2 are potential important ALS prognostic markers. Our findings provide evidence on the pathogenesis of ALS, potential targets for the development of new drugs for ALS, and important markers for predicting ALS prognosis. Full article
(This article belongs to the Special Issue Antioxidants and Anti-inflammatory Effects in Neurodegenerative Diseases)
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22 pages, 7189 KiB  
Article
Selected Kefir Water from Malaysia Attenuates Hydrogen Peroxide-Induced Oxidative Stress by Upregulating Endogenous Antioxidant Levels in SH-SY5Y Neuroblastoma Cells
by Muganti Rajah Kumar, Swee Keong Yeap, Han Chung Lee, Nurul Elyani Mohamad, Muhammad Nazirul Mubin Aziz, Melati Khalid, Mas Jaffri Masarudin, Adam Thean Chor Leow, Janna Ong Abdullah and Noorjahan Banu Alitheen
Antioxidants 2021, 10(6), 940; https://doi.org/10.3390/antiox10060940 - 10 Jun 2021
Cited by 13 | Viewed by 4323
Abstract
Kefir, a fermented probiotic drink was tested for its potential anti-oxidative, anti-apoptotic, and neuroprotective effects to attenuate cellular oxidative stress on human SH-SY5Y neuroblastoma cells. Here, the antioxidant potentials of the six different kefir water samples were analysed by total phenolic content (TPC), [...] Read more.
Kefir, a fermented probiotic drink was tested for its potential anti-oxidative, anti-apoptotic, and neuroprotective effects to attenuate cellular oxidative stress on human SH-SY5Y neuroblastoma cells. Here, the antioxidant potentials of the six different kefir water samples were analysed by total phenolic content (TPC), total flavonoid content (TFC), ferric reducing antioxidant power (FRAP), and 2,2′-diphenyl-1-picrylhydrazyl radical (DPPH) assays, whereas the anti-apoptotic activity on hydrogen peroxide (H2O2) induced SH-SY5Y cells was examined using MTT, AO/PI double staining, and PI/Annexin V-FITC assays. The surface and internal morphological features of SH-SY5Y cells were studied using scanning and transmission electron microscopy. The results indicate that Kefir B showed the higher TPC (1.96 ± 0.54 µg GAE/µL), TFC (1.09 ± 0.02 µg CAT eq/µL), FRAP (19.68 ± 0.11 mM FRAP eq/50 µL), and DPPH (0.45 ± 0.06 mg/mL) activities compared to the other kefir samples. The MTT and PI/Annexin V-FITC assays showed that Kefir B pre-treatment at 10 mg/mL for 48 h resulted in greater cytoprotection (97.04%), and a significantly lower percentage of necrotic cells (7.79%), respectively. The Kefir B pre-treatment also resulted in greater protection to cytoplasmic and cytoskeleton inclusion, along with the conservation of the surface morphological features and the overall integrity of SH-SY5Y cells. Our findings indicate that the anti-oxidative, anti-apoptosis, and neuroprotective effects of kefir were mediated via the upregulation of SOD and catalase, as well as the modulation of apoptotic genes (Tp73, Bax, and Bcl-2). Full article
(This article belongs to the Special Issue Antioxidants and Anti-inflammatory Effects in Neurodegenerative Diseases)
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20 pages, 5385 KiB  
Article
17-β Estradiol Rescued Immature Rat Brain against Glutamate-Induced Oxidative Stress and Neurodegeneration via Regulating Nrf2/HO-1 and MAP-Kinase Signaling Pathway
by Ibrahim Khan, Kamran Saeed, Min Gi Jo and Myeong Ok Kim
Antioxidants 2021, 10(6), 892; https://doi.org/10.3390/antiox10060892 - 1 Jun 2021
Cited by 23 | Viewed by 5387
Abstract
Dysregulated glutamate signaling, leading to neuronal excitotoxicity and death, has been associated with neurodegenerative pathologies. 17β-estradiol (E2) is a human steroid hormone having a role in reproduction, sexual maturation, brain health and biological activities. The study aimed to explain the neuroprotective role of [...] Read more.
Dysregulated glutamate signaling, leading to neuronal excitotoxicity and death, has been associated with neurodegenerative pathologies. 17β-estradiol (E2) is a human steroid hormone having a role in reproduction, sexual maturation, brain health and biological activities. The study aimed to explain the neuroprotective role of E2 against glutamate-induced ROS production, MAP kinase-dependent neuroinflammation, synaptic dysfunction and neurodegeneration in the cortex and hippocampus of postnatal day 7 rat brain. Biochemical and immunofluorescence analyses were applied. Our results showed that a single subcutaneous injection of glutamate (10 mg/kg) induced brain oxidative stress after 4 h by disturbing the homeostasis of glutathione (GSH) and revealed an upsurge in ROS and LPO levels and downregulated the expression of Nrf2 and HO-1 antioxidant protein. The glutamate-exposed P7 pups illustrated increased phosphorylation of stress-activated c-Jun N-terminal kinase (JNK) and p38 kinase (p38) and downregulated expression of P-Erk1/2. This was accompanied by pathological neuroinflammation as revealed by enhanced gliosis with upregulated expression of GFAP and Iba-1, and the activation of proinflammatory cytokines (TNF-α) in glutamate-injected P7 pups. Moreover, exogenous glutamate also reduced the expression of synaptic markers (PSD-95, SYP) and induced apoptotic neurodegeneration in the cortical and hippocampal regions by dysregulating the expression of Bax, Bcl-2 and caspase-3 in the developing rat brain. On the contrary, co-treatment of E2 (10 mg/kg) with glutamate significantly abrogated brain neuroinflammation, neurodegeneration and synapse loss by alleviating brain oxidative stress by upregulating the Nrf2/HO-1 antioxidant pathway and by deactivating pro-apoptotic P-JNK/P-p38 and activation of pro-survival P-Erk1/2 MAP kinase pathways. In brief, the data demonstrate the neuroprotective role of E2 against glutamate excitotoxicity-induced neurodegeneration. The study also encourages future studies investigating if E2 may be a potent neuroprotective and neurotherapeutic agent in different neurodegenerative diseases. Full article
(This article belongs to the Special Issue Antioxidants and Anti-inflammatory Effects in Neurodegenerative Diseases)
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15 pages, 2553 KiB  
Article
Hidrox® Roles in Neuroprotection: Biochemical Links between Traumatic Brain Injury and Alzheimer’s Disease
by Marika Cordaro, Angela Trovato Salinaro, Rosalba Siracusa, Ramona D’Amico, Daniela Impellizzeri, Maria Scuto, Maria Laura Ontario, Roberto Crea, Salvatore Cuzzocrea, Rosanna Di Paola, Roberta Fusco and Vittorio Calabrese
Antioxidants 2021, 10(5), 818; https://doi.org/10.3390/antiox10050818 - 20 May 2021
Cited by 35 | Viewed by 3895
Abstract
Traumatic brain injuries (TBI) are a serious public-health problem. Furthermore, subsequent TBI events can compromise TBI patients’ quality of life. TBI is linked to a number of long- and short-term complications such as cerebral atrophy and risk of developing dementia and Alzheimer’s Disease [...] Read more.
Traumatic brain injuries (TBI) are a serious public-health problem. Furthermore, subsequent TBI events can compromise TBI patients’ quality of life. TBI is linked to a number of long- and short-term complications such as cerebral atrophy and risk of developing dementia and Alzheimer’s Disease (AD). Following direct TBI damage, oxidative stress and the inflammatory response lead to tissue injury-associated neurodegenerative processes that are characteristic of TBI-induced secondary damage. Hidrox® showed positive effects in preclinical models of toxic oxidative stress and neuroinflammation; thus, the aim of this study was to evaluate the effect of Hidrox® administration on TBI-induced secondary injury and on the propagation of the AD-like neuropathology. Hidrox® treatment reduced histological damage after controlled cortical impact. Form a molecular point of view, hydroxytyrosol is able to preserve the cellular redox balance and protein homeostasis by activating the Nrf2 pathway and increasing the expression of phase II detoxifying enzymes such as HO-1, SOD, Catalase, and GSH, thus counteracting the neurodegenerative damage. Additionally, Hidrox® showed anti-inflammatory effects by reducing the activation of the NFkB pathway and related cytokines overexpression. From a behavioral point of view, Hidrox® treatment ameliorated the cognitive dysfunction and memory impairment induced by TBI. Additionally, Hidrox® was associated with a significant increased number of hippocampal neurons in the CA3 region, which were reduced post-TBI. In particular, Hidrox® decreased AD-like phenotypic markers such as ß-amyloid accumulation and APP and p-Tau overexpression. These findings indicate that Hidrox® could be a valuable treatment for TBI-induced secondary injury and AD-like pathological features. Full article
(This article belongs to the Special Issue Antioxidants and Anti-inflammatory Effects in Neurodegenerative Diseases)
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Review

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46 pages, 2160 KiB  
Review
Clinical and Preclinical Studies of Fermented Foods and Their Effects on Alzheimer’s Disease
by Muganti Rajah Kumar, Nor Farahin Azizi, Swee Keong Yeap, Janna Ong Abdullah, Melati Khalid, Abdul Rahman Omar, Mohd. Azuraidi Osman, Adam Thean Chor Leow, Sharifah Alawieyah Syed Mortadza and Noorjahan Banu Alitheen
Antioxidants 2022, 11(5), 883; https://doi.org/10.3390/antiox11050883 - 29 Apr 2022
Cited by 30 | Viewed by 6931
Abstract
The focus on managing Alzheimer’s disease (AD) is shifting towards prevention through lifestyle modification instead of treatments since the currently available treatment options are only capable of providing symptomatic relief marginally and result in various side effects. Numerous studies have reported that the [...] Read more.
The focus on managing Alzheimer’s disease (AD) is shifting towards prevention through lifestyle modification instead of treatments since the currently available treatment options are only capable of providing symptomatic relief marginally and result in various side effects. Numerous studies have reported that the intake of fermented foods resulted in the successful management of AD. Food fermentation is a biochemical process where the microorganisms metabolize the constituents of raw food materials, giving vastly different organoleptic properties and additional nutritional value, and improved biosafety effects in the final products. The consumption of fermented foods is associated with a wide array of nutraceutical benefits, including anti-oxidative, anti-inflammatory, neuroprotective, anti-apoptotic, anti-cancer, anti-fungal, anti-bacterial, immunomodulatory, and hypocholesterolemic properties. Due to their promising health benefits, fermented food products have a great prospect for commercialization in the food industry. This paper reviews the memory and cognitive enhancement and neuroprotective potential of fermented food products on AD, the recently commercialized fermented food products in the health and food industries, and their limitations. The literature reviewed here demonstrates a growing demand for fermented food products as alternative therapeutic options for the prevention and management of AD. Full article
(This article belongs to the Special Issue Antioxidants and Anti-inflammatory Effects in Neurodegenerative Diseases)
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18 pages, 994 KiB  
Review
Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease
by Shinichi Takahashi and Kyoko Mashima
Antioxidants 2022, 11(1), 170; https://doi.org/10.3390/antiox11010170 - 17 Jan 2022
Cited by 35 | Viewed by 6229
Abstract
Oxidative stress and neuroinflammation are common bases for disease onset and progression in many neurodegenerative diseases. In Parkinson disease, which is characterized by the degeneration of dopaminergic neurons resulting in dopamine depletion, the pathogenesis differs between hereditary and solitary disease forms and is [...] Read more.
Oxidative stress and neuroinflammation are common bases for disease onset and progression in many neurodegenerative diseases. In Parkinson disease, which is characterized by the degeneration of dopaminergic neurons resulting in dopamine depletion, the pathogenesis differs between hereditary and solitary disease forms and is often unclear. In addition to the pathogenicity of alpha-synuclein as a pathological disease marker, the involvement of dopamine itself and its interactions with glial cells (astrocyte or microglia) have attracted attention. Pacemaking activity, which is a hallmark of dopaminergic neurons, is essential for the homeostatic maintenance of adequate dopamine concentrations in the synaptic cleft, but it imposes a burden on mitochondrial oxidative glucose metabolism, leading to reactive oxygen species production. Astrocytes provide endogenous neuroprotection to the brain by producing and releasing antioxidants in response to oxidative stress. Additionally, the protective function of astrocytes can be modified by microglia. Some types of microglia themselves are thought to exacerbate Parkinson disease by releasing pro-inflammatory factors (M1 microglia). Although these inflammatory microglia may further trigger the inflammatory conversion of astrocytes, microglia may induce astrocytic neuroprotective effects (A2 astrocytes) simultaneously. Interestingly, both astrocytes and microglia express dopamine receptors, which are upregulated in the presence of neuroinflammation. The anti-inflammatory effects of dopamine receptor stimulation are also attracting attention because the functions of astrocytes and microglia are greatly affected by both dopamine depletion and therapeutic dopamine replacement in Parkinson disease. In this review article, we will focus on the antioxidative and anti-inflammatory effects of astrocytes and their synergism with microglia and dopamine. Full article
(This article belongs to the Special Issue Antioxidants and Anti-inflammatory Effects in Neurodegenerative Diseases)
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