Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.8
7.0
Journals
Antioxidants
Special Issues
Oxidative Stress and Inflammation in Movement Disorders
share announcement

Oxidative Stress and Inflammation in Movement Disorders

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 (30 April 2023) | Viewed by 16871

Special Issue Editors

Dr. Andrii Domanskyi

E-Mail Website
Guest Editor
Institute of Biotechnology, HiLIFE, University of Helsinki, 00014 Helsinki, Finland
Interests: Parkinson’s disease; protein aggregation; animal models; fibril-induced alpha-synuclein aggregation; human iPCS-derived neurons; viral vectors for somatic transgenesis; neurotrophic factors; neuroinflammation; autophagy-lysosomal system; neurodegeneration
Special Issues, Collections and Topics in MDPI journals
Dr. Rosanna Parlato

E-Mail Website
Guest Editor
Department of Neurology/Division of Neurodegenerative Disorders, Medical Faculty Mannheim University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany
Interests: Huntington’s disease; Parkinson’s disease; amyotropic lateral sclerosis; RNA metabolism; autophagy

Special Issue Information

Dear Colleagues,

Millions of people worldwide are suffering from incurable movement disorders, such as Parkinson’s, Huntington’s disease, ataxias, and amyotrophic lateral sclerosis. After a relatively long prodromal phase, patients progressively develop severe symptoms, and ultimately succumb to disease, facing inevitable death. As the disease causes and underlying mechanisms are beginning to be understood, today, the hope of finding disease-modifying treatments is higher than ever. Along with dysfunctional neurons and glia, the role of microglia, oxidative stress and inflammation in disease progression is being increasingly recognized and supported by a significant amount of experimental data. However, multiple open questions remain, regarding, for example, the imbalance between neuroprotective and cell-death-promoting processes during neuroinflammation at different disease stages. Despite failures in past clinical trials, treatments aiming to reduce oxidative stress and/or modulate inflammatory processes in the brain still hold great promise in attenuating the onset and progression of neurodegeneration. To ensure success, we need to deeply understand the molecular pathways driving disease progression, to identify compounds with appropriate pharmacological properties, and to apply them at correct time points.

We invite you to submit original research or review articles to this Special Issue, focusing on understanding the role of oxidative stress and inflammation in movement disorders. Submitted articles can include in vitro, in vivo and clinical studies relating to any of the following topics: causes of oxidative damage and inflammation, as well as the molecular and cellular response to oxidative damage in disease models and in patients; dysfunctional microglia in neurodegeneration; age-related and/or disease-specific changes in antioxidant defense and inflammatory pathways; and oxidative stress and inflammation biomarkers for diagnostics and monitoring disease progression and treatment efficacy.

We look forward to your contribution.

Dr. Andrii Domanskyi
Dr. Rosanna Parlato
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. 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

  • microglia
  • brain inflammation
  • reactive oxygen species
  • reactive nitrogen species
  • neurodegeneration
  • antioxidant therapy
  • oxidative stress/neuroinflammation biomarkers

Published Papers (5 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

16 pages, 2669 KiB  
Article
Leukocyte Telomere Length Variability as a Potential Biomarker in Patients with PolyQ Diseases
by Daniela Scarabino, Liana Veneziano, Alessia Fiore, Suran Nethisinghe, Elide Mantuano, Hector Garcia-Moreno, Gianmarco Bellucci, Nita Solanky, Maria Morello, Ginevra Zanni, Rosa Maria Corbo and Paola Giunti
Antioxidants 2022, 11(8), 1436; https://doi.org/10.3390/antiox11081436 - 24 Jul 2022
Cited by 3 | Viewed by 1538
Abstract
SCA1, SCA2, and SCA3 are the most common forms of SCAs among the polyglutamine disorders, which include Huntington’s Disease (HD). We investigated the relationship between leukocyte telomere length (LTL) and the phenotype of SCA1, SCA2, and SCA3, comparing them with HD. The results [...] Read more.
SCA1, SCA2, and SCA3 are the most common forms of SCAs among the polyglutamine disorders, which include Huntington’s Disease (HD). We investigated the relationship between leukocyte telomere length (LTL) and the phenotype of SCA1, SCA2, and SCA3, comparing them with HD. The results showed that LTL was significantly reduced in SCA1 and SCA3 patients, while LTL was significantly longer in SCA2 patients. A significant negative relationship between LTL and age was observed in SCA1 but not in SCA2 subjects. LTL of SCA3 patients depend on both patient’s age and disease duration. The number of CAG repeats did not affect LTL in the three SCAs. Since LTL is considered an indirect marker of an inflammatory response and oxidative damage, our data suggest that in SCA1 inflammation is present already at an early stage of disease similar to in HD, while in SCA3 inflammation and impaired antioxidative processes are associated with disease progression. Interestingly, in SCA2, contrary to SCA1 and SCA3, the length of leukocyte telomeres does not reduce with age. We have observed that SCAs and HD show a differing behavior in LTL for each subtype, which could constitute relevant biomarkers if confirmed in larger cohorts and longitudinal studies. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Movement Disorders)
►▼ Show Figures

Figure 1

Review

Jump to: Research

14 pages, 887 KiB  
Review
Oxidative Stress and Neuroinflammation in Parkinson’s Disease: The Role of Dopamine Oxidation Products
by Sasanka Chakrabarti and Marco Bisaglia
Antioxidants 2023, 12(4), 955; https://doi.org/10.3390/antiox12040955 - 18 Apr 2023
Cited by 6 | Viewed by 1976
Abstract
Parkinson’s disease (PD) is a chronic neurodegenerative condition affecting more than 1% of people over 65 years old. It is characterized by the preferential degeneration of nigrostriatal dopaminergic neurons, which is responsible for the motor symptoms of PD patients. The pathogenesis of this [...] Read more.
Parkinson’s disease (PD) is a chronic neurodegenerative condition affecting more than 1% of people over 65 years old. It is characterized by the preferential degeneration of nigrostriatal dopaminergic neurons, which is responsible for the motor symptoms of PD patients. The pathogenesis of this multifactorial disorder is still elusive, hampering the discovery of therapeutic strategies able to suppress the disease’s progression. While redox alterations, mitochondrial dysfunctions, and neuroinflammation are clearly involved in PD pathology, how these processes lead to the preferential degeneration of dopaminergic neurons is still an unanswered question. In this context, the presence of dopamine itself within this neuronal population could represent a crucial determinant. In the present review, an attempt is made to link the aforementioned pathways to the oxidation chemistry of dopamine, leading to the formation of free radical species, reactive quinones and toxic metabolites, and sustaining a pathological vicious cycle. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Movement Disorders)
►▼ Show Figures

Figure 1

30 pages, 1658 KiB  
Review
Potential Therapeutic Strategies for Skeletal Muscle Atrophy
by Li Huang, Ming Li, Chunyan Deng, Jiayi Qiu, Kexin Wang, Mengyuan Chang, Songlin Zhou, Yun Gu, Yuntian Shen, Wei Wang, Ziwei Huang and Hualin Sun
Antioxidants 2023, 12(1), 44; https://doi.org/10.3390/antiox12010044 - 26 Dec 2022
Cited by 14 | Viewed by 4822
Abstract
The maintenance of muscle homeostasis is vital for life and health. Skeletal muscle atrophy not only seriously reduces people’s quality of life and increases morbidity and mortality, but also causes a huge socioeconomic burden. To date, no effective treatment has been developed for [...] Read more.
The maintenance of muscle homeostasis is vital for life and health. Skeletal muscle atrophy not only seriously reduces people’s quality of life and increases morbidity and mortality, but also causes a huge socioeconomic burden. To date, no effective treatment has been developed for skeletal muscle atrophy owing to an incomplete understanding of its molecular mechanisms. Exercise therapy is the most effective treatment for skeletal muscle atrophy. Unfortunately, it is not suitable for all patients, such as fractured patients and bedridden patients with nerve damage. Therefore, understanding the molecular mechanism of skeletal muscle atrophy is crucial for developing new therapies for skeletal muscle atrophy. In this review, PubMed was systematically screened for articles that appeared in the past 5 years about potential therapeutic strategies for skeletal muscle atrophy. Herein, we summarize the roles of inflammation, oxidative stress, ubiquitin-proteasome system, autophagic-lysosomal pathway, caspases, and calpains in skeletal muscle atrophy and systematically expound the potential drug targets and therapeutic progress against skeletal muscle atrophy. This review focuses on current treatments and strategies for skeletal muscle atrophy, including drug treatment (active substances of traditional Chinese medicine, chemical drugs, antioxidants, enzyme and enzyme inhibitors, hormone drugs, etc.), gene therapy, stem cell and exosome therapy (muscle-derived stem cells, non-myogenic stem cells, and exosomes), cytokine therapy, physical therapy (electroacupuncture, electrical stimulation, optogenetic technology, heat therapy, and low-level laser therapy), nutrition support (protein, essential amino acids, creatine, β-hydroxy-β-methylbutyrate, and vitamin D), and other therapies (biomaterial adjuvant therapy, intestinal microbial regulation, and oxygen supplementation). Considering many treatments have been developed for skeletal muscle atrophy, we propose a combination of proper treatments for individual needs, which may yield better treatment outcomes. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Movement Disorders)
►▼ Show Figures

Graphical abstract

12 pages, 1432 KiB  
Review
Microglial Dysfunction in Neurodegenerative Diseases via RIPK1 and ROS
by Qiaoyan Wu and Chengyu Zou
Antioxidants 2022, 11(11), 2201; https://doi.org/10.3390/antiox11112201 - 07 Nov 2022
Cited by 3 | Viewed by 2123
Abstract
Microglial dysfunction is a major contributor to the pathogenesis of multiple neurodegenerative diseases. The neurotoxicity of microglia associated with oxidative stress largely depends on NF-κB pathway activation, which promotes the production and release of microglial proinflammatory cytokines and chemokines. In this review, we [...] Read more.
Microglial dysfunction is a major contributor to the pathogenesis of multiple neurodegenerative diseases. The neurotoxicity of microglia associated with oxidative stress largely depends on NF-κB pathway activation, which promotes the production and release of microglial proinflammatory cytokines and chemokines. In this review, we discuss the current literature on the essential role of the NF-κB pathway on microglial activation that exacerbates neurodegeneration, with a particular focus on RIPK1 kinase activity-dependent microglial dysfunction. As upregulated RIPK1 kinase activity is associated with reactive oxygen species (ROS) accumulation in neurodegenerative diseases, we also discuss the current knowledge about the mechanistic links between RIPK1 activation and ROS generation. Given RIPK1 kinase activity and oxidative stress are closely regulated with each other in a vicious cycle, future studies are required to be conducted to fully understand how RIPK1 and ROS collude together to disturb microglial homeostasis that drives neurodegenerative pathogenesis. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Movement Disorders)
►▼ Show Figures

Figure 1

24 pages, 980 KiB  
Review
Inflammation: Roles in Skeletal Muscle Atrophy
by Yanan Ji, Ming Li, Mengyuan Chang, Ruiqi Liu, Jiayi Qiu, Kexin Wang, Chunyan Deng, Yuntian Shen, Jianwei Zhu, Wei Wang, Lingchi Xu and Hualin Sun
Antioxidants 2022, 11(9), 1686; https://doi.org/10.3390/antiox11091686 - 29 Aug 2022
Cited by 47 | Viewed by 5798
Abstract
Various diseases can cause skeletal muscle atrophy, usually accompanied by inflammation, mitochondrial dysfunction, apoptosis, decreased protein synthesis, and enhanced proteolysis. The underlying mechanism of inflammation in skeletal muscle atrophy is extremely complex and has not been fully elucidated, thus hindering the development of [...] Read more.
Various diseases can cause skeletal muscle atrophy, usually accompanied by inflammation, mitochondrial dysfunction, apoptosis, decreased protein synthesis, and enhanced proteolysis. The underlying mechanism of inflammation in skeletal muscle atrophy is extremely complex and has not been fully elucidated, thus hindering the development of effective therapeutic drugs and preventive measures for skeletal muscle atrophy. In this review, we elaborate on protein degradation pathways, including the ubiquitin-proteasome system (UPS), the autophagy-lysosome pathway (ALP), the calpain and caspase pathways, the insulin growth factor 1/Akt protein synthesis pathway, myostatin, and muscle satellite cells, in the process of muscle atrophy. Under an inflammatory environment, various pro-inflammatory cytokines directly act on nuclear factor-κB, p38MAPK, and JAK/STAT pathways through the corresponding receptors, and then are involved in muscle atrophy. Inflammation can also indirectly trigger skeletal muscle atrophy by changing the metabolic state of other tissues or cells. This paper explores the changes in the hypothalamic-pituitary-adrenal axis and fat metabolism under inflammatory conditions as well as their effects on skeletal muscle. Moreover, this paper also reviews various signaling pathways related to muscle atrophy under inflammatory conditions, such as cachexia, sepsis, type 2 diabetes mellitus, obesity, chronic obstructive pulmonary disease, chronic kidney disease, and nerve injury. Finally, this paper summarizes anti-amyotrophic drugs and their therapeutic targets for inflammation in recent years. Overall, inflammation is a key factor causing skeletal muscle atrophy, and anti-inflammation might be an effective strategy for the treatment of skeletal muscle atrophy. Various inflammatory factors and their downstream pathways are considered promising targets for the treatment and prevention of skeletal muscle atrophy. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Movement Disorders)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop