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Oxidative Stress and Its Mitigation in Neurodegenerative Disorders

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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 (31 March 2026) | Viewed by 23363

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Prof. D. Allan Butterfield

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Department of Chemistry, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
Interests: aging; age-related disorders; oxidative stress; neurodegenerative disorders; Alzheimer's disease; brain

Special Issue Information

Dear Colleagues,

Oxidative stress, commonly defined as excessive production of free radicals, decreases the scavenging of free radicals by antioxidant enzymes and/or small-molecule antioxidants, and it is now widely accepted as a critical aspect of neuronal loss, with consequent abnormal pathology and symptomology, in neurodegenerative disorders. Among the latter disorders are Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis and Down syndrome.

In biological cells, the predominant indices of protein oxidation include excessive levels of protein-resident carbonyls or 3-nitrotyrosine, while the major indices of lipid peroxidation include protein-bound 4-hydroxynonenal (HNE), isoprostanes (mostly derived from peroxidation of arachidonic acid) and neuroprostanes (derived from the peroxidation of neuronal-resident docosahexaenoic acid). The major indices of the oxidation of DNA or RNA are 8-hydroxy-2-deoxyguanosine and 8-hydroxyguanosine, respectively.

The mechanisms of elevated oxidative stress are numerous and diverse, and they include mitochondrial dysfunction; metabolic dysfunction, including glucose dysfunction and insulin resistance and other metabolic processes; the activation of the mTORC1 pathway; the peroxidation of membrane bilayer-resident lipids; and roles involving the oligomeric forms of peptides, proteins and oligosaccharides.

Potential mitigation of oxidative stress can be achieved by certain endogenous antioxidant enzymes or small-molecule antioxidants, as well as by the application of exogenous small-molecule antioxidants, i.e., naturally occurring or synthetic molecules.

Papers discussing various aspects of oxidative stress and its mitigation in neurodegenerative disorders will be considered for inclusion in this Special Issue of Antioxidants.

Prof. D. Allan Butterfield
Guest Editor

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Keywords

oxidative stress
neurodegenerative disorders
brain
Alzheimer’s disease
Parkinson’s disease
Huntington’s disease

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Published Papers (11 papers)

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Research

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17 pages, 2307 KB

Open AccessArticle

Short-Chain Fatty Acids Enhance EAAT2-Mediated Glutamate Clearance and Alleviate Oxidative Stress in an MPTP Mouse Model of Parkinson’s Disease

by Weiqi Li, Jiali Li, Lulu Liu, Wenzhe Hu, Lei Wu, Songtao Ding, Bin Yu, Lin Jiang and Handeng Liu

Antioxidants 2025, 14(12), 1429; https://doi.org/10.3390/antiox14121429 - 27 Nov 2025

Cited by 2 | Viewed by 1291

Abstract

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuron loss, motor deficits, and oxidative stress. Emerging evidence suggests that short-chain fatty acids (SCFAs), microbial metabolites derived from gut fermentation, exert neuroprotective effects, but the underlying mechanisms remain incompletely understood. In this study, we investigated the role of SCFAs in modulating astrocytic glutamate clearance and oxidative stress in a PD mouse model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Behavioral tests demonstrated that SCFA treatment significantly improved locomotor activity, grip strength, and coordination, while attenuating dopaminergic neuron loss and tyrosine hydroxylase (TH) reduction in the substantia nigra and striatum. Mechanistically, SCFAs enhanced astrocytic glutamate uptake mediated by excitatory amino acid transporter 2 (EAAT2), suppressed astrocyte reactivity, and reduced neuroinflammation, as evidenced by decreased plasma interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α) levels. SCFAs also restored redox homeostasis by elevating glutathione, reducing malondialdehyde, preserving superoxide dismutase activity, and promoting nuclear factor-erythroid 2–related factor 2 (Nrf2) nuclear translocation with upregulation of downstream antioxidant enzymes like heme oxygenase-1 (HO-1), superoxide dismutase 1 (SOD1), and superoxide dismutase 2 (SOD2). Inhibition of EAAT2 with dihydrokainic acid (DHK) abolished the beneficial effects of SCFAs, highlighting the critical role of EAAT2 in mediating SCFA-driven neuroprotection. Collectively, our findings demonstrate that SCFAs confer neuroprotection in PD by enhancing EAAT2-dependent glutamate clearance, reducing reactive oxygen species (ROS) accumulation, and activating Nrf2-dependent antioxidant pathways, providing a mechanistic basis for SCFA-based therapeutic strategies in PD. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

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22 pages, 3518 KB

Open AccessArticle

Cannabinol’s Modulation of Genes Involved in Oxidative Stress Response and Neuronal Plasticity: A Transcriptomic Analysis

by Serena Silvestro, Marco Calabrò, Alessandra Trainito, Stefano Salamone, Federica Pollastro, Emanuela Mazzon and Aurelio Minuti

Antioxidants 2025, 14(6), 744; https://doi.org/10.3390/antiox14060744 - 17 Jun 2025

Viewed by 2025

Abstract

Cannabis sativa is a remarkable source of bioactive compounds, with over 150 distinct phytocannabinoids identified to date. Among these, cannabinoids are gaining attention as potential therapeutic agents for neurodegenerative diseases. Previous research showed that cannabinol (CBN), a minor cannabinoid derived from Δ⁹-tetrahydrocannabinol, exhibits antioxidant, anti-inflammatory, analgesic, and anti-bacterial effects. The objective of this study was to assess the protective potential of 24 h CBN pre-treatment, applied at different concentrations (5 µM, 10 µM, 20 µM, 50 µM, and 100 µM), in differentiated neuroblastoma × spinal cord (NSC-34) cells. Transcriptomic analysis was performed using next-generation sequencing techniques. Our results reveal that CBN had no negative impact on cell viability at the tested concentrations. Instead, it showed a significant effect on stress response and neuroplasticity-related processes. Specifically, based on the Reactome database, the biological pathways mainly perturbed by CBN pre-treatment were investigated. This analysis highlighted a significant enrichment in the Reactome pathway’s cellular response to stress, cellular response to stimuli, and axon guidance. Overall, our results suggest that CBN holds promise as an adjuvant agent for neurodegenerative diseases by modulating genes involved in neuronal cell survival and axon guidance. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

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Review

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21 pages, 339 KB

Open AccessReview

Translational Feasibility of Curcumin for Treatment of Alzheimer’s Disease: A Critical Appraisal of Clinical Challenges

by Jasmine Priya Virk, Malika G. Fernando, Prita Riana Asih and Ralph N. Martins

Antioxidants 2026, 15(5), 638; https://doi.org/10.3390/antiox15050638 - 18 May 2026

Viewed by 285

Abstract

The absence of robust and effective treatments for Alzheimer’s disease remains a major challenge in modern medicine. As one of the leading causes of death, its increasing prevalence and complex chronic pathogenesis impose a substantial societal and healthcare burden, intensifying the need for effective therapeutic strategies. Current treatments remain limited, with minimal impact on cognitive decline in symptomatic patients. Curcumin, the bioactive ingredient in turmeric, has taken precedence over other natural products due to its potent antioxidative and anti-inflammatory properties. Numerous publications have extensively reported on the therapeutic effect of curcumin in animal models of Alzheimer’s disease. However, no curcumin formulation has demonstrated consistent clinical efficacy against Alzheimer’s or other neurodegenerative diseases to date. Over the years, many critics have argued that curcumin’s undesirable chemical properties, mainly low bioavailability and rapid metabolism, pose significant barriers to its therapeutic use to target the brain. Considerable funding and research effort on emerging technologies such as nanoparticles and intranasal delivery continue to drive curcumin preclinical and clinical trials, prompting reflection on the rationale for continued investment. This narrative review critically dissects this disconnect, arguing that many purported benefits remain insufficiently substantiated, and identifying important opportunities where future research may hold promise for an effective treatment. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

28 pages, 2136 KB

Open AccessReview

Loss of Proteostasis and Early-Onset Neurodegeneration in Down Syndrome: From Mechanisms to Interventions

by Antonella Tramutola, Chiara Lanzillotta, Fabio Di Domenico, Eugenio Barone and Marzia Perluigi

Antioxidants 2026, 15(4), 520; https://doi.org/10.3390/antiox15040520 - 21 Apr 2026

Viewed by 696

Abstract

Down syndrome (DS), caused by trisomy 21, is the most prevalent genetic condition associated with accelerated aging and near-universal development of early-onset Alzheimer’s disease (AD). Beyond gene-dosage imbalance, trisomy 21 induces widespread transcriptional, metabolic, and proteomic remodeling that establishes a chronic state of proteotoxic and oxidative stress from early development. Increasing evidence identifies DS as a disorder of proteostasis network failure, in which sustained translational pressure, redox disequilibrium, and degradation pathway insufficiency progressively erode cellular resilience. In the DS brain, persistent endoplasmic reticulum stress with PERK-dominant signaling, mitochondrial dysfunction characterized by oxidative phosphorylation deficits and excessive reactive oxygen species production, and impaired antioxidant responses create a highly vulnerable intracellular environment. Concomitantly, degradation systems become compromised: proteasomal catalytic activity declines, ubiquitin-dependent signaling is remodeled, and chronic mTOR hyperactivation suppresses autophagic and mitophagic flux. The coordinated impairment of the ubiquitin–proteasome system and autophagy establish a feed-forward cycle of proteotoxic accumulation and redox amplification. Within this framework, Alzheimer-like neuropathology in DS emerges not solely from amyloid precursor protein triplication but as the late manifestation of decades-long proteostasis exhaustion. Therapeutic strategies aimed at restoring global proteostasis and redox balance may therefore represent a more effective systems-level approach to mitigating neurodegeneration in DS. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

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29 pages, 1442 KB

Open AccessReview

Potential Protection Against Parkinson’s Disease by Ergothioneine—Nature’s Multifactorial Neuroprotectant

by Teddy J. W. Tng, Irwin K. Cheah, Barry Halliwell and Kah-Leong Lim

Antioxidants 2026, 15(4), 519; https://doi.org/10.3390/antiox15040519 - 21 Apr 2026

Viewed by 1608

Abstract

The use of neuroprotective nutraceuticals as a strategy against neurodegenerative diseases such as Parkinson’s disease (PD) has gained considerable traction in recent years. In this review, we highlight ergothioneine (ET)—a naturally occurring thiol/thione derivative abundant in mushrooms—as a promising candidate, given its long half-life, blood–brain barrier penetration, and high bioavailability. Numerous population studies have linked low blood ET levels with increased risk and progression of neurological and other age-related disorders in humans, suggesting that dietary ET may confer neuroprotective benefits. Supporting this, several studies have demonstrated the efficacy of ET treatment in reducing PD-associated molecular damage across various pre-clinical models such as C. elegans, Drosophila, rodent models and human neuronal cultures, leading to marked improvements in disease phenotypes. Here, we summarize some of the proposed mechanisms by which ET may exert neuroprotection in PD, including the reduction of protein aggregation, enhancement of mitochondrial function, mitigation of oxidative stress, and attenuation of apoptosis and neuroinflammation. We also highlight recent clinical trials demonstrating the safety and potential efficacy of ET and propose future research to facilitate the translation of ET into the clinic. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

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24 pages, 718 KB

Open AccessReview

Natural Vitamins and Novel Synthetic Antioxidants Targeting Mitochondria in Cognitive Health: A Scoping Review of In Vivo Evidence

by Alexia Squillace, Malika G. Fernando, Kirstin Sullivan, Hosen Kiat and Ralph N. Martins

Antioxidants 2026, 15(1), 78; https://doi.org/10.3390/antiox15010078 - 7 Jan 2026

Viewed by 1450

Abstract

Mitochondrial dysfunction and oxidative stress are crucial contributors to the pathogenesis of Alzheimer’s disease (AD) and dementia exhibiting cognitive decline at the early stage of neurodegeneration. Natural vitamin antioxidants (NVAs) and novel mitochondria-targeted antioxidants (MTAs) are proposed as potential therapeutics though conclusive evidence is lacking. Objectives were to examine in vivo evidence on NVAs and MTAs for preventing and/or treating cognitive decline leading to dementia, to identify the most promising antioxidants, and highlight translational gaps. Methods followed PRISMA-ScR guidelines. MEDLINE, EMBASE and Scopus were searched for English language in vivo experiments assessing NVAs or MTAs in AD and dementia. A total of 25 studies (13 NVAs; 12 MTAs) met inclusion criteria. NVAs (Vitamin A, B, C, E) demonstrated mixed efficacy in reducing oxidative stress and improving cognitive outcomes, with Vitamin E showing the most consistent neuroprotective effects. MTAs (MitoQ, MitoTEMPO, SS31, SkQ1) improved mitochondrial dynamics and cognitive performance and reduced dementia-related pathology. Both NVAs and MTAs improved biomarker profiles and cognitive outcomes in vivo animal models of AD and dementia, but MTAs showed more robust and consistent efficacy by directly targeting mitochondrial pathways. Given the favourable safety profiles of MTAs in other clinical conditions, early-phase human trials in dementia and AD are warranted to evaluate their long-term cognitive benefits. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

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34 pages, 2440 KB

Open AccessReview

Protective Functions of β-Alanyl-L-Histidine and Glycyl-L-Histidyl-L-Lysine Glycoconjugates and Copper in Concert

by Irina Naletova and Enrico Rizzarelli

Antioxidants 2025, 14(12), 1512; https://doi.org/10.3390/antiox14121512 - 17 Dec 2025

Viewed by 2223

Abstract

Two endogenous peptides, β-alanyl-L-histidine, named carnosine (Car), and glycyl-L-histidyl-L-lysine (GHK), derived from the matricellular protein Secreted Protein Acidic and Rich in Cysteine (SPARC), share many beneficial functions. The hydrolytic enzyme carnosinase for Car and the low stability for GHK can put into question their antioxidant, antiaggregating, and anti-inflammatory properties. The glycoconjugates of Car with a di- (trehalose, Tre) or polysaccharide (hyaluronan, HA) inhibit carnosinase, while the synthesis of HAGHK derivatives increases the tripeptide stability and protects/delays the biopolymer degradation. A synergic effect between the two components of the glycoconjugates is evident in their consequently preserved protective features. TreCar, HACar, and HAGHK maintain the copper-binding ability of the peptides alone, and the saccharides potentiate the Cu,Zn-superoxide dismutase-like ability of the copper(II) complexes with the glycoconjugates. These peptide derivatives behave as copper ionophores, utilizing Cu²⁺ present in the culture medium; also, an increase in the metal intracellular level occurs with a consequent stimulation of the copper-driven signaling pathways that produce the expression/release of trophic (Brain-Derived Neurotrophic Factor, BDNF, and Bone Morphogenetic Protein 2, BMP-2) and angiogenic (Vascular Endothelial Growth Factor, VEGF) proteins. Copper chaperons for SOD1, CCS, and Antioxidant 1 (Atox-1) are the copper chaperones that act as transcription factors. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

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22 pages, 608 KB

Open AccessReview

The Heme Oxygenase/Biliverdin Reductase System as a Therapeutic Target to Counteract Cellular Senescence in Alzheimer’s Disease

by Cesare Mancuso

Antioxidants 2025, 14(10), 1237; https://doi.org/10.3390/antiox14101237 - 15 Oct 2025

Viewed by 1829

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder involving free radical overload, neuroinflammation, and a deranged cell stress response. In particular, the modulation of the heme oxygenase/biliverdin reductase (HO/BVR) system, a key component of the brain stress response, is currently regarded as a promising therapeutic approach for AD. Cellular senescence, defined as a process of cell cycle arrest due to oxidative stress, DNA damage, mitochondrial dysfunction, and oncogene activation, has been identified as a pivotal factor in the development of AD. A mounting body of research has demonstrated that the accumulation of senescent cells in the brain can lead to a variety of neurotoxic effects, including synaptic dysfunction, the destruction of the blood–brain barrier, and impaired remyelination. Finally, the release of proinflammatory molecules by senescent cells further exacerbates neurodegeneration. A considerable number of xenobiotics, with well-documented neuroprotective effects through the activation of the HO/BVR system, have been shown to modulate pathways involved in cellular senescence outside the brain. Unfortunately, a direct link between HO/BVR and cellular senescence in AD is yet to be established. This compelling evidence should motivate basic and clinical researchers to address such a significant gap in knowledge and conduct novel studies in this field. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

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13 pages, 723 KB

Open AccessReview

Oxidative Stress, Advanced Glycation End Products (AGEs), and Neurodegeneration in Alzheimer’s Disease: A Metabolic Perspective

by Virginia Boccardi, Francesca Mancinetti and Patrizia Mecocci

Antioxidants 2025, 14(9), 1044; https://doi.org/10.3390/antiox14091044 - 25 Aug 2025

Cited by 17 | Viewed by 6499

Abstract

Neurodegenerative diseases such as Alzheimer’s disease (AD) are closely linked to oxidative stress and advanced glycation end products (AGEs), two interrelated processes that exacerbate neuronal damage through mitochondrial dysfunction, protein aggregation, and chronic inflammation. This narrative review explores the metabolic interplay between reactive oxygen species (ROS) and AGEs, with a focus on the AGE-RAGE (receptor for advanced glycation end products) signaling axis as a driver of neurodegeneration. Evidence from preclinical and clinical studies highlights their combined role in disease progression and underscores potential therapeutic targets. Strategies including mitochondria-targeted antioxidants, AGE inhibitors, RAGE antagonists, and metabolic interventions are discussed, along with future directions for biomarker development and personalized treatments. This review integrates current molecular insights into a unified metabolic–inflammatory model of AD, highlighting translational therapeutic opportunities. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

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24 pages, 3218 KB

Open AccessReview

Biological Models of Oxidative Purine DNA Damage in Neurodegenerative Disorders

by Chryssostomos Chatgilialoglu

Antioxidants 2025, 14(5), 578; https://doi.org/10.3390/antiox14050578 - 11 May 2025

Cited by 5 | Viewed by 2942

Abstract

Most DNA damage caused by oxidative metabolism consists of single lesions that can accumulate in tissues. This review focuses on two classes of lesions: the two 8-oxopurine (8-oxo-Pu) lesions that are repaired by the base excision repair (BER) enzyme and the four 5′,8-cyclopurine (cPu) lesions that are repaired exclusively by the nucleotide excision repair (NER) enzyme. The aim is to correlate the simultaneous quantification of these two classes of lesions in the context of neurological disorders. The first half is a summary of reactive oxygen species (ROS) with particular attention to the pathways of hydroxyl radical (HO^•) formation, followed by a summary of protocols for the quantification of six lesions and the biomimetic chemistry of the HO^• radical with double-stranded oligonucleotides (ds-ODN) and calf thymus DNA (ct-DNA). The second half addresses two neurodegenerative diseases: xeroderma pigmentosum (XP) and Cockayne syndrome (CS). The quantitative data on the six lesions obtained from genomic and/or mitochondrial DNA extracts across several XP and CS cell lines are discussed. Oxidative stress contributes to oxidative DNA damage by resulting in the accumulation of cPu and 8-oxo-Pu in DNA. The formation of cPu is the postulated culprit inducing neurological symptoms associated with XP and CS. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

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Other

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11 pages, 716 KB

Open AccessPerspective

Microbial Metabolism of Levodopa as an Adjunct Therapeutic Target in Parkinson’s Disease

by Jimmy B. Feix, Gang Cheng, Micael Hardy and Balaraman Kalyanaraman

Antioxidants 2026, 15(1), 120; https://doi.org/10.3390/antiox15010120 - 17 Jan 2026

Cited by 1 | Viewed by 1174

Abstract

Parkinson’s disease is the second leading neurodegenerative disease of aging. For over five decades, oral levodopa has been used to manage the progressive motor deficits that are the hallmark of the disease. However, individual dose requirements are highly variable, and patients typically require increased levodopa dosage as the disease progresses, which can cause undesirable side effects. It has become increasingly apparent that the gut microbiome can have a major impact on the metabolism and efficacy of therapeutic drugs. In this Perspective, we examine recent studies highlighting the impact of metabolism by Enterococcus faecalis, a common commensal gut bacterium, on levodopa bioavailability. E. faecalis expresses a highly conserved tyrosine decarboxylase that promiscuously converts levodopa to dopamine in the gut, resulting in decreased neuronal uptake of levodopa and reduced dopamine formation in the brain. Mitochondria-targeted antioxidants conjugated to a triphenylphosphonium moiety have shown promise in transiently suppressing the growth of E. faecalis and decreasing microbial levodopa metabolism, providing an approach to modulating the microbiome that is less perturbing than conventional antibiotics. Thus, mitigating metabolism by the gut microbiota is an attractive therapeutic target to preserve and potentiate the efficacy of oral levodopa therapy in Parkinson’s disease. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

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