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Antioxidants
Special Issues
Redox Metals and Catecholamines in Neurodegenerative Diseases
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Redox Metals and Catecholamines 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 (10 January 2025) | Viewed by 4636

Special Issue Editors

Prof. Dr. Enrico Monzani

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Guest Editor
Dipartimento di Chimica, Università di Pavia, Via Taramelli 12, 27100 Pavia, Italy
Interests: redox chemistry; neurodegenerative diseases; neurodegeneration
Dr. Chiara Bacchella

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Guest Editor
Dipartimento di Chimica, Università di Pavia, Via Taramelli 12, 27100 Pavia, Italy
Interests: metal complexes; coordination chemistry; catalysis; neurodegeneration

Special Issue Information

Dear Colleagues,

Alteration in metal levels is detected in different pathophysiological mechanisms associated with neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD) and multiple sclerosis (MS). The imbalance of some essential metals, including zinc (Zn), copper (Cu), iron (Fe) and manganese (Mn), compromises structures and functions of several proteins and enzymes, promoting neurotoxicity, mitochondrial dysregulation and cell death. Another pathological mechanism usually reviewed as pivotal in neurodegeneration involves catecholamine oxidation-derived neurodamage. Catecholamines such as dopamine, epinephrine and norepinephrine are reactive molecules prone to undergo dioxygen-dependent self-oxidation and metal-catalyzed oxidation. These oxidative pathways can give rise to unspecific protein modifications, resulting in structural misfolding, inactivation and aggregation into insoluble neuro-deposits.

This Special Issue aims to provide the basis for a better understanding of the metals and catecholamine-related biochemical mechanisms that trigger these neurodisorders. We invite investigators to submit original papers focused on the topics outlined below:

  • Catecholamine reactivity and interplay with redox active metals
  • Catecholamine oxidative products and metals as neuronal biomarkers
  • Catecholamine-mediated modification of proteins and peptides
  • Neuroinflammation promoted by trace metals
  • Recent advances in drug discovery based on metal and catecholamine-related pathways.

Prof. Dr. Enrico Monzani
Dr. Chiara Bacchella
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

  • neurodegeneration
  • catecholamines
  • redox metals
  • oxidative stress
  • protein modification

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Published Papers (3 papers)

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Research

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19 pages, 2034 KiB  
Article
Protective Contribution of Rosmarinic Acid in Rosemary Extract Against Copper-Induced Oxidative Stress
by Arian Kola, Ginevra Vigni, Stefania Lamponi and Daniela Valensin
Antioxidants 2024, 13(11), 1419; https://doi.org/10.3390/antiox13111419 - 19 Nov 2024
Cited by 3 | Viewed by 2053
Abstract
Rosemary extract (Rosmarinus officinalis) is a natural source of bioactive compounds with significant antioxidant properties. Among these, rosmarinic acid is celebrated for its potent antioxidant, anti-inflammatory, antimicrobial, and neuroprotective properties, making it a valuable component in both traditional medicine and modern [...] Read more.
Rosemary extract (Rosmarinus officinalis) is a natural source of bioactive compounds with significant antioxidant properties. Among these, rosmarinic acid is celebrated for its potent antioxidant, anti-inflammatory, antimicrobial, and neuroprotective properties, making it a valuable component in both traditional medicine and modern therapeutic research. Neurodegenerative diseases like Alzheimer’s and Parkinson’s are closely linked to oxidative damage, and research indicates that rosmarinic acid may help protect neurons by mitigating this harmful process. Rosmarinic acid is able to bind cupric ions (Cu2+) and interfere with the production of reactive oxygen species (ROS) produced by copper through Fenton-like reactions. This study aims to further evaluate the contribution of rosmarinic acid within rosemary extract by comparing its activity to that of isolated rosmarinic acid. By using a detailed approach that includes chemical characterization, antioxidant capacity assessment, and neuroprotective activity testing, we have determined whether the combined components in rosemary extract enhance or differ from the effects of rosmarinic acid alone. This comparison is crucial for understanding whether the full extract offers added benefits beyond those of isolated rosmarinic acid in combating oxidative stress and Aβ-induced toxicity. Full article
(This article belongs to the Special Issue Redox Metals and Catecholamines in Neurodegenerative Diseases)
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Review

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23 pages, 7219 KiB  
Review
A Focus on the Link Between Metal Dyshomeostasis, Norepinephrine, and Protein Aggregation
by Chiara Bacchella, Andrea Capucciati and Enrico Monzani
Antioxidants 2025, 14(3), 347; https://doi.org/10.3390/antiox14030347 - 15 Mar 2025
Viewed by 543
Abstract
Neurodegenerative disorders are one of the main public health problems worldwide and, for this reason, they have attracted the attention of several researchers who aim to better understand the molecular processes linked to the etiology of these disorders, including Alzheimer’s and Parkinson’s diseases. [...] Read more.
Neurodegenerative disorders are one of the main public health problems worldwide and, for this reason, they have attracted the attention of several researchers who aim to better understand the molecular processes linked to the etiology of these disorders, including Alzheimer’s and Parkinson’s diseases. In this review, we describe both the beneficial and toxic effect of norepinephrine (NE) and its connected ROS/metal-mediated pathways, which end in neuromelanin (NM) formation and protein aggregation. In particular, we emphasize the importance of stabilizing the delicate homeostatic balance that regulates (i) the metal/ROS-promoted oxidation of catecholamines, as NE, and (ii) the generation of oxidative by-products capable of covalently and non-covalently modifying neuroproteins, thus altering their stability and their oligomerization; these processes may end in (iii) the incorporation of protein conjugates into vesicles, which then evolve into neuromelanin (NM) organelles. In general, we aim to provide an up-to-date overview of the challenges and controversies emerging from the current literature to delineate a direction for future research. Full article
(This article belongs to the Special Issue Redox Metals and Catecholamines in Neurodegenerative Diseases)
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17 pages, 1527 KiB  
Review
Fading Blue: Exploring the Causes of Locus Coeruleus Damage Across the Lifespan
by Alessandro Galgani, Marco Scotto, Ugo Faraguna and Filippo S. Giorgi
Antioxidants 2025, 14(3), 255; https://doi.org/10.3390/antiox14030255 - 22 Feb 2025
Viewed by 897
Abstract
Locus Coeruleus (LC) is a brain nucleus that is involved in a variety of key functions (ranging from attention modulation to sleep–wake cycle regulation, to memory encoding); its proper function is necessary both during brain development and for brain integrity maintenance, and both [...] Read more.
Locus Coeruleus (LC) is a brain nucleus that is involved in a variety of key functions (ranging from attention modulation to sleep–wake cycle regulation, to memory encoding); its proper function is necessary both during brain development and for brain integrity maintenance, and both at the microscale and macroscale level. Due to their specific intrinsic and extrinsic features, LC cells are considered particularly susceptible to damage concerning a variety of insults. This explains LC involvement in degenerative diseases not only in adults (in the context of neurodegenerative disease, mainly), but also in children (in relation to early hypoxic damage and Down’s Syndrome, among others). In this narrative review, we dissect the potential mechanisms through which LC is affected in different diseases, with a special emphasis on the high rate of activity it is subjected to and the oxidative stress associated with it. Further research aimed at deepening our understanding of these mechanisms is needed to enable the development of potential strategies in the future that could slow down LC degeneration in subjects predisposed to specific brain disorders. Full article
(This article belongs to the Special Issue Redox Metals and Catecholamines in Neurodegenerative Diseases)
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