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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: 15 September 2024 | Viewed by 3560

Special Issue Editor

Dr. J. Josh Lawrence

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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

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.

Published Papers (2 papers)

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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 1 | Viewed by 1573
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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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
Viewed by 1580
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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