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Antioxidants
Special Issues
Oxidative Stress and Alzheimer’s Disease
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Oxidative Stress and Alzheimer’s Disease

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 (15 September 2024) | Viewed by 7076

Special Issue Editor

Dr. J. Josh Lawrence

E-Mail Website
Guest Editor
Department of Pharmacology and Neuroscience, Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, USA
Interests: nutrigenomics, cellular and synaptic physiology of Alzheimer’s disease; role of excitation/inhibition balance in disease states, hippocampal learning and memory circuitry; GABAergic inhibition; cell type specificity of neuromodulation; antioxidant depletion over lifespan; neuroinflammation; effects of diet on healthy aging; computational neuroscience; bioinformatics

Special Issue Information

Dear Colleagues,

Oxidative stress (OS) occurs through the generation of reactive oxygen species (ROS), causing damage to lipids, proteins, and DNA. Antioxidants function as ROS scavengers, limiting the damage produced by excess ROS. Lipid peroxidation and antioxidant depletion were historically discovered in blood from Alzheimer’s disease (AD) patients, raising the possibility that OS mechanisms contribute to AD pathogenesis and progression. As antioxidant depletion exacerbates OS, it is likely that the prodromal “silent” period of AD involves antioxidant depletion, shifting the redox balance subtly over years through the oxidation of ion channels, leading to the early stages of AD. There is also an interplay between exogenous and endogenous antioxidants, whereby antioxidant defenses are triggered when the redox balance is disrupted. However, the mobilization of antioxidant defenses and DNA repair mechanisms cannot reverse AD progression, ultimately leading to the homeostatic collapse of antioxidant defenses in AD. Finally, the effectiveness of extent antioxidant supplementation has mixed results in the literature. Antioxidant-related transcription factors may be unable to access specific response elements on DNA that has been damaged across the lifespan or with AD. This Special Issue encourages the submission of articles related to these areas in order to strengthen our understanding of the molecular mechanisms underlying oxidative stress and antioxidant depletion in various stages of AD.

Dr. J. Josh Lawrence
Guest Editor

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Published Papers (4 papers)

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Research

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21 pages, 4788 KiB  
Article
Betula pendula Leaf Extract Targets the Interplay between Brain Oxidative Stress, Inflammation, and NFkB Pathways in Amyloid Aβ1-42-Treated Rats
by Alexandra-Cristina Sevastre-Berghian, Irina Ielciu, Timea Bab, Neli-Kinga Olah, Vlad Sever Neculicioiu, Vlad Alexandru Toma, Bogdan Sevastre, Teodora Mocan, Daniela Hanganu, Andreea Elena Bodoki, Ioana Roman, Roxana Liana Lucaciu, Adriana Corina Hangan, Alina-Diana Hașaș, Roxana Maria Decea and Ioana Băldea
Antioxidants 2023, 12(12), 2110; https://doi.org/10.3390/antiox12122110 - 13 Dec 2023
Cited by 3 | Viewed by 2282
Abstract
Alzheimer’s disease (AD) is known as the primary and most common cause of dementia in the middle-aged and elderly population worldwide. Chemical analyses of B. pendula leaf extract (BPE), performed using spectrophotometric and chromatographic methods (LC/MS), revealed high amounts of polyphenol carboxylic acids [...] Read more.
Alzheimer’s disease (AD) is known as the primary and most common cause of dementia in the middle-aged and elderly population worldwide. Chemical analyses of B. pendula leaf extract (BPE), performed using spectrophotometric and chromatographic methods (LC/MS), revealed high amounts of polyphenol carboxylic acids (gallic, chlorogenic, caffeic, trans-p-coumaric, ferulic, and salicylic acids), as well as flavonoids (apigenin, luteolin, luteolin-7-O-glucoside, naringenin, hyperoside, quercetin, and quercitrin). Four groups of Wistar rats were used in this experiment (n = 7/group): control (untreated), Aβ1-42 (2 μg/rat intracerebroventricular (i.c.v.), Aβ1-42 + BPE (200 mg/Kg b.w.), and DMSO (10 μL/rat). On the first day, one dose of Aβ1-42 was intracerebroventricularly administered to animals in groups 2 and 3. Subsequently, BPE was orally administered for the next 15 days to group 3. On the 16th day, behavioral tests were performed. Biomarkers of brain oxidative stress Malondialdehyde (MDA), (Peroxidase (PRx), Catalase (CAT), and Superoxid dismutase (SOD) and inflammation (cytokines: tumor necrosis factor -α (TNF-α), Interleukin 1β (IL-1β), and cyclooxygenase-2 (COX 2)) in plasma and hippocampus homogenates were assessed. Various protein expressions (Phospho-Tau (Ser404) (pTau Ser 404), Phospho-Tau (Ser396) (pTau Ser 396), synaptophysin, and the Nuclear factor kappa B (NFkB) signaling pathway) were analyzed using Western blot and immunohistochemistry in the hippocampus. The results show that BPE diminished lipid peroxidation and neuroinflammation, modulated specific protein expression, enhanced the antioxidant capacity, and improved spontaneous alternation behavior, suggesting that it has beneficial effects in AD. Full article
(This article belongs to the Special Issue Oxidative Stress and Alzheimer’s Disease)
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Review

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27 pages, 1765 KiB  
Review
Potential Roles of Hypoxia-Inducible Factor-1 in Alzheimer’s Disease: Beneficial or Detrimental?
by Tsu-Kung Lin, Chi-Ren Huang, Kai-Jung Lin, Yi-Heng Hsieh, Shang-Der Chen, Yi-Chun Lin, A-Ching Chao and Ding-I Yang
Antioxidants 2024, 13(11), 1378; https://doi.org/10.3390/antiox13111378 - 11 Nov 2024
Viewed by 645
Abstract
The major pathological characteristics of Alzheimer’s disease (AD) include senile plaques and neurofibrillary tangles (NFTs), which are mainly composed of aggregated amyloid-beta (Aβ) peptide and hyperphosphorylated tau protein, respectively. The excessive production of reactive oxygen species (ROS) and neuroinflammation are crucial contributing factors [...] Read more.
The major pathological characteristics of Alzheimer’s disease (AD) include senile plaques and neurofibrillary tangles (NFTs), which are mainly composed of aggregated amyloid-beta (Aβ) peptide and hyperphosphorylated tau protein, respectively. The excessive production of reactive oxygen species (ROS) and neuroinflammation are crucial contributing factors to the pathological mechanisms of AD. Hypoxia-inducible factor-1 (HIF-1) is a transcription factor critical for tissue adaption to low-oxygen tension. Growing evidence has suggested HIF-1 as a potential therapeutic target for AD; conversely, other experimental findings indicate that HIF-1 induction contributes to AD pathogenesis. These previous findings thus point to the complex, even contradictory, roles of HIF-1 in AD. In this review, we first introduce the general pathogenic mechanisms of AD as well as the potential pathophysiological roles of HIF-1 in cancer, immunity, and oxidative stress. Based on current experimental evidence in the literature, we then discuss the possible beneficial as well as detrimental mechanisms of HIF-1 in AD; these sections also include the summaries of multiple chemical reagents and proteins that have been shown to exert beneficial effects in AD via either the induction or inhibition of HIF-1. Full article
(This article belongs to the Special Issue Oxidative Stress and Alzheimer’s Disease)
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38 pages, 2727 KiB  
Review
Mitochondrial Quality Control in Alzheimer’s Disease: Insights from Caenorhabditis elegans Models
by Upasana Ganguly, Trae Carroll, Keith Nehrke and Gail V. W. Johnson
Antioxidants 2024, 13(11), 1343; https://doi.org/10.3390/antiox13111343 - 1 Nov 2024
Viewed by 1209
Abstract
Alzheimer’s disease (AD) is a complex neurodegenerative disorder that is classically defined by the extracellular deposition of senile plaques rich in amyloid-beta (Aβ) protein and the intracellular accumulation of neurofibrillary tangles (NFTs) that are rich in aberrantly modified tau protein. In addition to [...] Read more.
Alzheimer’s disease (AD) is a complex neurodegenerative disorder that is classically defined by the extracellular deposition of senile plaques rich in amyloid-beta (Aβ) protein and the intracellular accumulation of neurofibrillary tangles (NFTs) that are rich in aberrantly modified tau protein. In addition to aggregative and proteostatic abnormalities, neurons affected by AD also frequently possess dysfunctional mitochondria and disrupted mitochondrial maintenance, such as the inability to eliminate damaged mitochondria via mitophagy. Decades have been spent interrogating the etiopathogenesis of AD, and contributions from model organism research have aided in developing a more fundamental understanding of molecular dysfunction caused by Aβ and toxic tau aggregates. The soil nematode C. elegans is a genetic model organism that has been widely used for interrogating neurodegenerative mechanisms including AD. In this review, we discuss the advantages and limitations of the many C. elegans AD models, with a special focus and discussion on how mitochondrial quality control pathways (namely mitophagy) may contribute to AD development. We also summarize evidence on how targeting mitophagy has been therapeutically beneficial in AD. Lastly, we delineate possible mechanisms that can work alone or in concert to ultimately lead to mitophagy impairment in neurons and may contribute to AD etiopathology. Full article
(This article belongs to the Special Issue Oxidative Stress and Alzheimer’s Disease)
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30 pages, 4150 KiB  
Review
The Contribution of Hippocampal All-Trans Retinoic Acid (ATRA) Deficiency to Alzheimer’s Disease: A Narrative Overview of ATRA-Dependent Gene Expression in Post-Mortem Hippocampal Tissue
by Joey Almaguer, Ashly Hindle and J. Josh Lawrence
Antioxidants 2023, 12(11), 1921; https://doi.org/10.3390/antiox12111921 - 27 Oct 2023
Cited by 2 | Viewed by 2166
Abstract
There is accumulating evidence that vitamin A (VA) deficiency contributes to the pathogenesis and progression of Alzheimer’s disease (AD). All-trans retinoic acid (ATRA), a metabolite of VA in the brain, serves distinct roles in the human hippocampus. Agonists of retinoic acid receptors [...] Read more.
There is accumulating evidence that vitamin A (VA) deficiency contributes to the pathogenesis and progression of Alzheimer’s disease (AD). All-trans retinoic acid (ATRA), a metabolite of VA in the brain, serves distinct roles in the human hippocampus. Agonists of retinoic acid receptors (RAR), including ATRA, promote activation of the non-amyloidogenic pathway by enhancing expression of α-secretases, providing a mechanistic basis for delaying/preventing amyloid beta (Aβ) toxicity. However, whether ATRA is actually deficient in the hippocampi of patients with AD is not clear. Here, using a publicly available human transcriptomic dataset, we evaluated the extent to which ATRA-sensitive genes are dysregulated in hippocampal tissue from post-mortem AD brains, relative to age-matched controls. Consistent with ATRA deficiency, we found significant dysregulation of many ATRA-sensitive genes and significant upregulation of RAR co-repressors, supporting the idea of transcriptional repression of ATRA-mediated signaling. Consistent with oxidative stress and neuroinflammation, Nrf2 and NfkB transcripts were upregulated, respectively. Interestingly, transcriptional targets of Nrf2 were not upregulated, accompanied by upregulation of several histone deacetylases. Overall, our investigation of ATRA-sensitive genes in the human hippocampus bolsters the scientific premise of ATRA depletion in AD and that epigenetic factors should be considered and addressed as part of VA supplementation. Full article
(This article belongs to the Special Issue Oxidative Stress and Alzheimer’s Disease)
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