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Antioxidants
Special Issues
Energy Disorders in Neurodegenerative Diseases
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Energy Disorders 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 (30 December 2021) | Viewed by 7329

Special Issue Editors

Prof. Dr. Wojciech Kozubski

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Guest Editor
Chair and Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
Interests: neurodegenerative diseases; neuroscience; neurobiology; pharmacotherapy effects; genetics
Prof. Jolanta Dorszewska

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Guest Editor
Laboratory of Neurobiology, Department of Neurology, Poznan University of Medical Sciences, 60965 Poznan, Poland
Interests: Neurodegenerative diseases, Neuroscience, Neurobiology, Pharmacotherapy Effects, Genetics

Special Issue Information

Dear Colleagues,

It is now believed that one of the causes of central neuron damage is increasing oxidative stress. The reason for its generation is the central deposition of pathological proteins such as amyloid-beta in Alzheimer’s disease, alpha-synuclein in Parkinson’s disease, and huntingtin in Huntington’s disease. Abnormal levels and/or structure of pathological proteins are often the result of genetic variants in the genes encoding them. In addition, abnormal proteins level may lead to disturbances in energy homeostasis, e.g. by the weakening of the complexes of the respiratory chains, I in Parkinson's disease, IV in Alzheimer's disease, and VI in normal aging, as well as altering mitochondrial function. The level of endogenous such as glutathione (GSH) or superoxide dismutase 1 (SOD1) and exogenous antioxidants are also important for maintaining energy homeostasis. Abnormalities in GSH levels in Alzheimer’s disease and altered SOD1 activity in amyotrophic lateral sclerosis have been demonstrated. The level of GSH is regulated by the efficiency of the transsulfuration of biothiol, homocysteine, into cysteine. Disorders of biothiols metabolism showed in both Alzheimer's and Parkinson's disease.

Although it is known oxidative stress accompanies many diseases and is associated with the processes of normal aging. However, we do not know for sure whether oxidative stress is an effect or the main cause of the aging changes and diseases of the central nervous system.

This research topic will be presented in preclinical and clinical studies showing the participation of energy disorders in the manifestation and development of common neurodegenerative diseases.

Prof. Dr. Wojciech Kozubski
Prof. Jolanta Dorszewska
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

  • Genetics
  • Pathological proteins
  • Respiratory chain complexes
  • Mitochondria
  • Antioxidants
  • Biothiols
  • Alzheimer’s disease
  • Parkinson’s disease
  • Amyotrophic lateral sclerosis
  • Huntington disease
  • Normal aging

Published Papers (2 papers)

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Review

19 pages, 2364 KiB  
Review
Iron Dysregulation in Mitochondrial Dysfunction and Alzheimer’s Disease
by John O. Onukwufor, Robert T. Dirksen and Andrew P. Wojtovich
Antioxidants 2022, 11(4), 692; https://doi.org/10.3390/antiox11040692 - 31 Mar 2022
Cited by 31 | Viewed by 4103
Abstract
Alzheimer’s disease (AD) is a devastating progressive neurodegenerative disease characterized by neuronal dysfunction, and decreased memory and cognitive function. Iron is critical for neuronal activity, neurotransmitter biosynthesis, and energy homeostasis. Iron accumulation occurs in AD and results in neuronal dysfunction through activation of [...] Read more.
Alzheimer’s disease (AD) is a devastating progressive neurodegenerative disease characterized by neuronal dysfunction, and decreased memory and cognitive function. Iron is critical for neuronal activity, neurotransmitter biosynthesis, and energy homeostasis. Iron accumulation occurs in AD and results in neuronal dysfunction through activation of multifactorial mechanisms. Mitochondria generate energy and iron is a key co-factor required for: (1) ATP production by the electron transport chain, (2) heme protein biosynthesis and (3) iron-sulfur cluster formation. Disruptions in iron homeostasis result in mitochondrial dysfunction and energetic failure. Ferroptosis, a non-apoptotic iron-dependent form of cell death mediated by uncontrolled accumulation of reactive oxygen species and lipid peroxidation, is associated with AD and other neurodegenerative diseases. AD pathogenesis is complex with multiple diverse interacting players including Aβ-plaque formation, phosphorylated tau, and redox stress. Unfortunately, clinical trials in AD based on targeting these canonical hallmarks have been largely unsuccessful. Here, we review evidence linking iron dysregulation to AD and the potential for targeting ferroptosis as a therapeutic intervention for AD. Full article
(This article belongs to the Special Issue Energy Disorders in Neurodegenerative Diseases)
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23 pages, 1292 KiB  
Review
Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy
by Ryszard Pluta, Jacek Kiś, Sławomir Januszewski, Mirosław Jabłoński and Stanisław J. Czuczwar
Antioxidants 2022, 11(1), 146; https://doi.org/10.3390/antiox11010146 - 11 Jan 2022
Cited by 15 | Viewed by 2649
Abstract
Recent years have seen remarkable progress in research into free radicals oxidative stress, particularly in the context of post-ischemic recirculation brain injury. Oxidative stress in post-ischemic tissues violates the integrity of the genome, causing DNA damage, death of neuronal, glial and vascular cells, [...] Read more.
Recent years have seen remarkable progress in research into free radicals oxidative stress, particularly in the context of post-ischemic recirculation brain injury. Oxidative stress in post-ischemic tissues violates the integrity of the genome, causing DNA damage, death of neuronal, glial and vascular cells, and impaired neurological outcome after brain ischemia. Indeed, it is now known that DNA damage and repair play a key role in post-stroke white and gray matter remodeling, and restoring the integrity of the blood-brain barrier. This review will present one of the newly characterized mechanisms that emerged with genomic and proteomic development that led to brain ischemia to a new level of post-ischemic neuropathological mechanisms, such as the presence of amyloid plaques and the development of neurofibrillary tangles, which further exacerbate oxidative stress. Finally, we hypothesize that modified amyloid and the tau protein, along with the oxidative stress generated, are new key elements in the vicious circle important in the development of post-ischemic neurodegeneration in a type of Alzheimer’s disease proteinopathy. Full article
(This article belongs to the Special Issue Energy Disorders in Neurodegenerative Diseases)
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