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Cells
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Oxidative Stress in Aging and Neurodegenerative Diseases
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Oxidative Stress in Aging and Neurodegenerative Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 18553

Special Issue Editor

Dr. Xudong Huang

E-Mail Website
Guest Editor
Neurochemistry Lab, Department of Psychiatry, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Charlestown, MA 02129, USA
Interests: aging; exposome and exposomics; Alzheimer’s disease; Parkinson’s disease; depression; artificial intelligence; machine and deep learning; big data analytics; blockchain; stigma, socially assistive robotics; virtual/augmented/mixed reality; cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

A plethora of experimental and clinical research data have indicated that oxidative stress has contributed to aging and related neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Lou Gehrig's disease or Amyotrophic lateral sclerosis (ALS), etc. As such, further understanding of pathological mechanisms involving oxidative stress in aging and neurodegenerative diseases may help with developing targeted antioxidant therapies for aging and age-associated neurodegenerative diseases. Thus, we are pleased to invite you to contribute to our Special Issue- “Oxidative Stress in Aging and Neurodegenerative Diseases”. This Special Issue aims to featuring oxidative stress research in the field of aging and related neurodegenerative diseases. We hope that this Special Issue will serve as an ideal forum for dissemination innovative research (including clinical research), current advancement, and ideas in the field. In this Special Issue, original research articles and reviews are welcome. Research areas may include (but not limited to) the following:

  • Oxidative stress in aging
  • Oxidative stress in Alzheimer’s disease
  • Oxidative stress in Parkinson’s disease
  • Oxidative stress in Lou Gehrig's disease
  • Anti-oxidative stress drug discovery
  • Targeted Antioxidant Therapy
  • Molecular imaging methods and agents for oxidative stress

I look forward to receiving your contributions. 

You may choose our Joint Special Issue in Geriatrics.

Dr. Xudong Huang
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • aging
  • oxidative stress
  • antioxidant
  • Alzheimer’s disease
  • Parkinson’s disease
  • Lou Gehrig’s disease
  • drug discovery

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Related Special Issue

Published Papers (6 papers)

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Research

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12 pages, 2068 KiB  
Article
A Preliminary Study of Mild Heat Stress on Inflammasome Activation in Murine Macrophages
by Simmie L. Foster, Abigail J. Dutton, Adina Yerzhan, Lindsay B. March, Katherine Barry, Corey R. Seehus, Xudong Huang, Sebastien Talbot and Clifford J. Woolf
Cells 2023, 12(8), 1189; https://doi.org/10.3390/cells12081189 - 19 Apr 2023
Cited by 4 | Viewed by 1969
Abstract
Inflammation and mitochondrial-dependent oxidative stress are interrelated processes implicated in multiple neuroinflammatory disorders, including Alzheimer’s disease (AD) and depression. Exposure to elevated temperature (hyperthermia) is proposed as a non-pharmacological, anti-inflammatory treatment for these disorders; however, the underlying mechanisms are not fully understood. Here [...] Read more.
Inflammation and mitochondrial-dependent oxidative stress are interrelated processes implicated in multiple neuroinflammatory disorders, including Alzheimer’s disease (AD) and depression. Exposure to elevated temperature (hyperthermia) is proposed as a non-pharmacological, anti-inflammatory treatment for these disorders; however, the underlying mechanisms are not fully understood. Here we asked if the inflammasome, a protein complex essential for orchestrating the inflammatory response and linked to mitochondrial stress, might be modulated by elevated temperatures. To test this, in preliminary studies, immortalized bone-marrow-derived murine macrophages (iBMM) were primed with inflammatory stimuli, exposed to a range of temperatures (37–41.5 °C), and examined for markers of inflammasome and mitochondrial activity. We found that exposure to mild heat stress (39 °C for 15 min) rapidly inhibited iBMM inflammasome activity. Furthermore, heat exposure led to decreased ASC speck formation and increased numbers of polarized mitochondria. These results suggest that mild hyperthermia inhibits inflammasome activity in the iBMM, limiting potentially harmful inflammation and mitigating mitochondrial stress. Our findings suggest an additional potential mechanism by which hyperthermia may exert its beneficial effects on inflammatory diseases. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Neurodegenerative Diseases)
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14 pages, 4087 KiB  
Article
Fullerenols Prevent Neuron Death and Reduce Oxidative Stress in Drosophila Huntington’s Disease Model
by Olga I. Bolshakova, Alina A. Borisenkova, Ilya M. Golomidov, Artem E. Komissarov, Alexandra D. Slobodina, Elena V. Ryabova, Irina S. Ryabokon, Evgenia M. Latypova, Elizaveta E. Slepneva and Svetlana V. Sarantseva
Cells 2023, 12(1), 170; https://doi.org/10.3390/cells12010170 - 31 Dec 2022
Cited by 7 | Viewed by 2859
Abstract
Huntington’s disease (HD) is one of the human neurodegenerative diseases for which there is no effective treatment. Therefore, there is a strong demand for a novel neuroprotective agent that can alleviate its course. Fullerene derivatives are considered to be such agents; however, they [...] Read more.
Huntington’s disease (HD) is one of the human neurodegenerative diseases for which there is no effective treatment. Therefore, there is a strong demand for a novel neuroprotective agent that can alleviate its course. Fullerene derivatives are considered to be such agents; however, they need to be comprehensively investigated in model organisms. In this work, neuroprotective activity of C60(OH)30 and C120O(OH)44 fullerenols was analyzed for the first time in a Drosophila transgenic model of HD. Lifespan, behavior, oxidative stress level and age-related neurodegeneration were assessed in flies with the pathogenic Huntingtin protein expression in nerve cells. Feed supplementation with hydroxylated C60 fullerene and C120O dimer oxide molecules was shown to diminish the oxidative stress level and neurodegenerative processes in the flies’ brains. Thus, fullerenes displayed neuroprotective activity in this model. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Neurodegenerative Diseases)
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Review

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12 pages, 2319 KiB  
Review
A Concise Review on Oxidative Stress-Mediated Ferroptosis and Cuproptosis in Alzheimer’s Disease
by Xudong Huang
Cells 2023, 12(10), 1369; https://doi.org/10.3390/cells12101369 - 12 May 2023
Cited by 10 | Viewed by 3411
Abstract
Alzheimer’s disease (AD), which was first identified more than a century ago, has become a pandemic that exacts enormous social burden and economic tolls as no measure of combating devastated AD is currently available. Growing etiopathological, genetic, and biochemical data indicate that AD [...] Read more.
Alzheimer’s disease (AD), which was first identified more than a century ago, has become a pandemic that exacts enormous social burden and economic tolls as no measure of combating devastated AD is currently available. Growing etiopathological, genetic, and biochemical data indicate that AD is a heterogeneous, polygenic, multifactorial, and complex disease. However, its exact etiopathology remains to be determined. Numerous experimental data show that cerebral iron and copper dyshomeostasis contribute to Aβ amyloidosis and tauopathy, two neuropathological hallmarks of AD. Moreover, increasing experimental evidence suggests ferroptosis, an iron-dependent and nonapoptotic form of cell death, may be involved in the neurodegenerative process in the AD brain. Thus, the anti-ferroptosis approach may be an efficacious therapeutic strategy for AD patients. Furthermore, it remains to be further determined whether cuproptosis, a copper-dependent and distinct form of regulated cell death, also plays a contributing role in AD neurodegeneration. We hope this concise review of recent experimental studies of oxidative stress-mediated ferroptosis and cuproptosis in AD may spur further investigations on this timely and essential line of research. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Neurodegenerative Diseases)
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60 pages, 15175 KiB  
Review
The Neuroprotective Activities of the Novel Multi-Target Iron-Chelators in Models of Alzheimer’s Disease, Amyotrophic Lateral Sclerosis and Aging
by Lana Kupershmidt and Moussa B. H. Youdim
Cells 2023, 12(5), 763; https://doi.org/10.3390/cells12050763 - 27 Feb 2023
Cited by 16 | Viewed by 3296
Abstract
The concept of chelation therapy as a valuable therapeutic approach in neurological disorders led us to develop multi-target, non-toxic, lipophilic, brain-permeable compounds with iron chelation and anti-apoptotic properties for neurodegenerative diseases, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), age-related dementia and amyotrophic [...] Read more.
The concept of chelation therapy as a valuable therapeutic approach in neurological disorders led us to develop multi-target, non-toxic, lipophilic, brain-permeable compounds with iron chelation and anti-apoptotic properties for neurodegenerative diseases, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), age-related dementia and amyotrophic lateral sclerosis (ALS). Herein, we reviewed our two most effective such compounds, M30 and HLA20, based on a multimodal drug design paradigm. The compounds have been tested for their mechanisms of action using animal and cellular models such as APP/PS1 AD transgenic (Tg) mice, G93A-SOD1 mutant ALS Tg mice, C57BL/6 mice, Neuroblastoma × Spinal Cord-34 (NSC-34) hybrid cells, a battery of behavior tests, and various immunohistochemical and biochemical techniques. These novel iron chelators exhibit neuroprotective activities by attenuating relevant neurodegenerative pathology, promoting positive behavior changes, and up-regulating neuroprotective signaling pathways. Taken together, these results suggest that our multifunctional iron-chelating compounds can upregulate several neuroprotective-adaptive mechanisms and pro-survival signaling pathways in the brain and might function as ideal drugs for neurodegenerative disorders, such as PD, AD, ALS, and aging-related cognitive decline, in which oxidative stress and iron-mediated toxicity and dysregulation of iron homeostasis have been implicated. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Neurodegenerative Diseases)
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16 pages, 870 KiB  
Review
Crosstalk between Oxidative Stress and Aging in Neurodegeneration Disorders
by Rehab F. Abdelhamid and Seiichi Nagano
Cells 2023, 12(5), 753; https://doi.org/10.3390/cells12050753 - 27 Feb 2023
Cited by 18 | Viewed by 3011
Abstract
The world population is aging rapidly, and increasing lifespan exacerbates the burden of age-related health issues. On the other hand, premature aging has begun to be a problem, with increasing numbers of younger people suffering aging-related symptoms. Advanced aging is caused by a [...] Read more.
The world population is aging rapidly, and increasing lifespan exacerbates the burden of age-related health issues. On the other hand, premature aging has begun to be a problem, with increasing numbers of younger people suffering aging-related symptoms. Advanced aging is caused by a combination of factors: lifestyle, diet, external and internal factors, as well as oxidative stress (OS). Although OS is the most researched aging factor, it is also the least understood. OS is important not only in relation to aging but also due to its strong impact on neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), Alzheimer’s disease (AD), and Parkinson’s disease (PD). In this review, we will discuss the aging process in relation to OS, the function of OS in neurodegenerative disorders, and prospective therapeutics capable of relieving neurodegenerative symptoms associated with the pro-oxidative condition. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Neurodegenerative Diseases)
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16 pages, 1860 KiB  
Review
Recent Advances in the Study of Na+/K+-ATPase in Neurodegenerative Diseases
by Xiaoyan Zhang, Weithye Lee and Jin-Song Bian
Cells 2022, 11(24), 4075; https://doi.org/10.3390/cells11244075 - 16 Dec 2022
Cited by 17 | Viewed by 2873
Abstract
Na+/K+-ATPase (NKA), a large transmembrane protein, is expressed in the plasma membrane of most eukaryotic cells. It maintains resting membrane potential, cell volume and secondary transcellular transport of other ions and neurotransmitters. NKA consumes about half of the ATP [...] Read more.
Na+/K+-ATPase (NKA), a large transmembrane protein, is expressed in the plasma membrane of most eukaryotic cells. It maintains resting membrane potential, cell volume and secondary transcellular transport of other ions and neurotransmitters. NKA consumes about half of the ATP molecules in the brain, which makes NKA highly sensitive to energy deficiency. Neurodegenerative diseases (NDDs) are a group of diseases characterized by chronic, progressive and irreversible neuronal loss in specific brain areas. The pathogenesis of NDDs is sophisticated, involving protein misfolding and aggregation, mitochondrial dysfunction and oxidative stress. The protective effect of NKA against NDDs has been emerging gradually in the past few decades. Hence, understanding the role of NKA in NDDs is critical for elucidating the underlying pathophysiology of NDDs and identifying new therapeutic targets. The present review focuses on the recent progress involving different aspects of NKA in cellular homeostasis to present in-depth understanding of this unique protein. Moreover, the essential roles of NKA in NDDs are discussed to provide a platform and bright future for the improvement of clinical research in NDDs. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Neurodegenerative Diseases)
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