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Advancing Personalized Medicine: Targeting Oxidative Stress in Neurodegenerative Diseases
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Advancing Personalized Medicine: Targeting Oxidative Stress in Neurodegenerative Diseases

A Special Issue of Journal of Personalized Medicine (ISSN 2075-4426) belonging to the section "Mechanisms of Diseases".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 7941

Editor

Dr. Lucia Buccarello

E-Mail Website
Guest Editor
1. Saint Camillus International University of Health and Medical Sciences, Via di Sant’Alessandro, Rome, Italy
2. European Brain Research Institute-Fondazione Rita Levi-Montalcini, Rome, Italy
Interests: neurodegeneration; cell death; neuroprotection; neuronal death; intracellular signaling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The rising prevalence of neurodegenerative disorders, significantly influenced by epigenetic factors, underscores the urgent need for personalized medicine approaches that integrate innovative technologies to enhance clinical treatment efficacy. Oxidative stress, which is characterized by an imbalance between reactive oxygen and nitrogen species and antioxidant defenses, plays a pivotal role in the pathogenesis of these disorders. However, the mechanisms underlying this imbalance remain incompletely understood. Addressing these processes through personalized medicine strategies could offer promising therapeutic avenues for various neurodegenerative conditions.

This Special Issue will consolidate efforts from both the medical and research communities to investigate and clarify the contribution of oxidative stress in neurodegenerative diseases. Our objective is to identify novel therapeutic strategies for early detection, diagnosis, risk assessment, and treatment through personalized medicine approaches. Your contributions will be essential in providing new knowledge to tackle neurodegenerative diseases and in making the few available treatments more effective through a personalized medicine approach.

We will consider original research, systematic reviews, and experimental pre-clinical and clinical studies that explore the role of personalized medicine in addressing oxidative stress in neurodegenerative disorders.

Relevant topics include the following:

  • Alzheimer's disease;
  • Parkinson's disease;
  • Amyotrophic lateral sclerosis;
  • Huntington's disease;
  • Mitochondrial dysfunction;
  • Neuroinflammation;
  • Neuronal death;
  • Impaired protein degradation pathways;
  • Novel biomarkers for neurodegenerative diseases;
  • Emerging therapies in neurodegenerative diseases;
  • Neuroprotective strategies.

We particularly encourage submissions that employ innovative methodologies such as genomics, pharmacogenomics, artificial intelligence-driven predictive models, transcriptomics, proteomics, and machine learning models for patient stratification. These approaches are essential for advancing precision medicine in the context of oxidative stress and neurodegenerative diseases.

Dr. Lucia Buccarello
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Personalized Medicine 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 2600 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.

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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14 pages, 1911 KB  
Article
Protection Against Cellular Toxicity from Rotenone Treatment by the Neuroprotective, Novel Multifunctional Antiparkinsonian Drug D-512
by Pranay Ravipati, Liping Xu, Deepthi Yedlapudi and Aloke K. Dutta
J. Pers. Med. 2026, 16(2), 115; https://doi.org/10.3390/jpm16020115 - 14 Feb 2026
Viewed by 1671
Abstract
Objective: Exposure to rotenone, a naturally occurring pesticide, has been linked to an increased risk of developing Parkinson’s disease (PD). Rotenone strongly inhibits complex I of the mitochondrial respiratory chain, inducing oxidative stress both in vitro and in vivo, ultimately leading to [...] Read more.
Objective: Exposure to rotenone, a naturally occurring pesticide, has been linked to an increased risk of developing Parkinson’s disease (PD). Rotenone strongly inhibits complex I of the mitochondrial respiratory chain, inducing oxidative stress both in vitro and in vivo, ultimately leading to cell death. The objective of this study was to evaluate the cytoprotective effects of the multifunctional agonist D-512 against rotenone-induced toxicity in neuronal PC12 and dopaminergic MN9D cell lines. Methods: Various cell-based assays, including cell viability, antioxidant activity, caspase-mediated apoptosis, and other related assays, were performed. Results: Rotenone was found to be toxic to both dopaminergic MN9D cells and neuronal PC12 cells. However, treatment with D-512 protected both cell types from rotenone-induced toxicity in a dose-dependent manner. Rotenone-induced impairment of mitochondrial membrane potential and increased production of reactive oxygen species were reversed by D-512 treatment. Furthermore, rotenone-induced caspase-mediated apoptotic signaling in MN9D cells was inhibited by D-512. In addition, D-512 restored levels of phosphorylated tyrosine hydroxylase in rotenone-exposed cells across various doses, indicating protection of the dopaminergic system. Finally, rotenone-induced activation of phosphorylated ERK was reversed by D-512 treatment, further supporting its neuroprotective potential. Conclusions: This study demonstrates the ability of D-512 to reverse the toxic effects of rotenone across multiple experimental models. The data presented here are consistent with previously reported neuroprotective properties of D-512. The multifunctional nature of D-512, which combines potent dopamine agonist activity with neuroprotective and other beneficial properties, may address therapeutic needs in PD beyond symptomatic relief and could have potential application across PD subgroups as part of a personalized therapeutic approach. Full article
(This article belongs to the Special Issue Advancing Personalized Medicine: Targeting Oxidative Stress in Neurodegenerative Diseases)
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Review

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34 pages, 2612 KB  
Review
The Bright and Dark Sides of Nitric Oxide in Neurodegenerative Diseases
by Lucia Buccarello, Costanza Montagna, Sabina Di Matteo, Renata Mangione, Giuseppe Carota, Jay Sibbitts, Romana Jarosova, Susan M. Lunte, Giacomo Lazzarino and Giuseppe Caruso
J. Pers. Med. 2026, 16(5), 246; https://doi.org/10.3390/jpm16050246 - 1 May 2026
Cited by 2 | Viewed by 2512
Abstract
Nitric oxide (NO) plays an important role in neuronal communication, synaptic plasticity and vascular regulation. Due to its important function in neuronal homeostasis, NO imbalance is associated with neurodegeneration. Specifically, in Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD) and frontotemporal [...] Read more.
Nitric oxide (NO) plays an important role in neuronal communication, synaptic plasticity and vascular regulation. Due to its important function in neuronal homeostasis, NO imbalance is associated with neurodegeneration. Specifically, in Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD) and frontotemporal lobar degeneration (FTLD), an excessive amount of NO, mostly produced by inducible NO synthase (iNOS), reacts with superoxide to form peroxynitrite, driving oxidative/nitrosative stress, mitochondrial dysfunction, and aberrant protein modifications. In AD, NO dysregulation promotes amyloid-β (Aβ) accumulation, tau hyperphosphorylation and synaptic loss, creating a self-perpetuating cycle of neuronal damage. NO’s dual role, protective at physiological levels but harmful if overproduced, underscores the therapeutic potential of antioxidant compounds that restore the balance of NO/NOS (especially iNOS) while preserving physiological functions. However, despite the emerging role of antioxidant-based therapeutic approaches, clinical translation is limited by the complexity of NO signaling and the absence of safe, specific NOS inhibitors. By targeting the molecular switch from protective to toxic, NO activity may offer new personalized treatment avenues for neurodegenerative diseases. Full article
(This article belongs to the Special Issue Advancing Personalized Medicine: Targeting Oxidative Stress in Neurodegenerative Diseases)
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15 pages, 563 KB  
Review
The Role of Oxidative Stress in the Relationship Between Periodontitis and Alzheimer’s Disease: A Review of the Literature
by Konstantinos Antonios Papadakis, Aikaterini-El Doufexi, Mary S. Kalamaki, Evangelos Bourazanas and Evgenia Lymperaki
J. Pers. Med. 2025, 15(8), 384; https://doi.org/10.3390/jpm15080384 - 18 Aug 2025
Cited by 16 | Viewed by 3176
Abstract
Periodontitis, a chronic inflammatory disease affecting the supporting tissues of the teeth, has been linked to the onset of neurological diseases, including Alzheimer’s disease (AD). A primary mechanism connecting these two issues is oxidative stress caused by an imbalance between antioxidant defenses and [...] Read more.
Periodontitis, a chronic inflammatory disease affecting the supporting tissues of the teeth, has been linked to the onset of neurological diseases, including Alzheimer’s disease (AD). A primary mechanism connecting these two issues is oxidative stress caused by an imbalance between antioxidant defenses and reactive oxygen species (ROS) synthesis. This review compiles results from both animal and human studies that explore how oxidative stress resulting from periodontitis leads to neuroinflammation, mitochondrial dysfunction, and cognitive decline in AD. Studies in animals indicate that periodontal infections worsen brain oxidative damage, as evidenced by elevated lipid peroxidation markers, such as malondialdehyde (MDA), and indicators of oxidative DNA damage, including 8-hydroxy-2′-deoxyguanosine (8-OHdG). Additionally, significant reductions in crucial antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase, along with neuroinflammation and cognitive deficits, are observed in mouse models of induced periodontitis. Supporting evidence from human studies reveals lower total antioxidant capacity (TAC) in individuals with both Alzheimer’s disease (AD) and periodontitis, as well as increased systemic oxidative stress markers, such as advanced oxidation protein products (AOPRs). These findings suggest a mechanistic relationship through oxidative stress pathways between periodontal inflammation and neurodegeneration. Given the extensive impact of periodontitis, enhancing periodontal health could be a viable strategy to reduce oxidative damage and lower the risk of cognitive decline. Further research is needed to clarify causality and to investigate antioxidant treatments aimed at preventing or slowing the progression of AD in patients with periodontal disease. Full article
(This article belongs to the Special Issue Advancing Personalized Medicine: Targeting Oxidative Stress in Neurodegenerative Diseases)
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