Special Issue "Marine Organisms with Neuroprotective Activity: Molecular Targets and Action Mechanisms"

A special issue of Marine Drugs (ISSN 1660-3397).

Deadline for manuscript submissions: 30 October 2019.

Special Issue Editors

Guest Editor
Prof. Dr. Lydia Giménez-Llort Website E-Mail
Institut de Neurociències, Department of Psychiatry & Forensic Medicine, Faculty of Medicine, Campus Bellaterra, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Barcelona, Spain
Interests: Alzheimer's disease; neurodegenerative diseases; translational behavioral neuroscience and pharmacology; aging; behavioral neuroendocrinology; neuropharmacology
Guest Editor
Prof. Dr. Luis M. Botana Website E-Mail
Department of Pharmacology, Faculty of Veterinary, University of Santiago of Compostela, 27002 Lugo, Spain
Phone: 34982822233
Interests: pharmacology; analytical biochemistry; signal transduction; compound isolation

Special Issue Information

Dear Colleagues,

Marine compounds have shown an extreme diversity in both chemical structure and modes of action. There is no doubt that the future of neuroprotection will include several natural or derived marine compounds, as the literature is now suggesting. The privileged structures provided by marine organisms bring about the question of why they are producing this variety of compounds so active in mammals, but their use is potentially very promising, not only in terms of action, but also because their molecular size and kinetics favor their development as drug leads.

This Special Issue of marine organisms with neuroprotective activity seeks to highlight the potential of marine drugs for neuroprotection, with a special emphasis on the diversity of molecular targets and mechanistic effects. Original (in vitro, animal, and clinical), review, and conceptual articles on known and novel bioactive marine products with potential neuroprotective activity and its translational value are encouraged.

Prof. Dr. Lydia Giménez-Llort
Prof. Dr. Luis M. Botana
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 papers will be 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. Marine Drugs 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 2000 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

  • Marine toxins
  • Sponges
  • Neuroprotection
  • Molecular targets
  • Mechanisms of action
  • Translational research

Published Papers (4 papers)

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Research

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Open AccessArticle
Testing the Neuroprotective Properties of PCSO-524® Using a Neuronal Cell Cycle Suppression Assay
Mar. Drugs 2019, 17(2), 79; https://doi.org/10.3390/md17020079 - 24 Jan 2019
Abstract
Cell cycle reentry is a unified mechanism shared by several neurodegenerative diseases, including Alzheimer’s disease (AD) and Ataxia Telangiectasia (A-T). This phenotype is often related to neuroinflammation in the central nervous system. To mimic brain inflammation in vitro, we adopted the previously established [...] Read more.
Cell cycle reentry is a unified mechanism shared by several neurodegenerative diseases, including Alzheimer’s disease (AD) and Ataxia Telangiectasia (A-T). This phenotype is often related to neuroinflammation in the central nervous system. To mimic brain inflammation in vitro, we adopted the previously established method of using conditioned medium collected from activated THP-1 cells and applied it to both differentiated HT22 cells and primary neurons. Unscheduled cell cycle events were observed in both systems, indicating the potential of this approach as an in vitro model of neurodegenerative disease. We used this assay to measure the neuroprotective effects of New Zealand green-lipped mussel extract, PCSO-524®, to protect post-mitotic cells from cell cycle reentry. We found that, both in vitro and in an animal model, PCSO-524® displayed promising neuroprotective effects, and thus has potential to postpone or prevent the onset of neurodegenerative disease. Full article
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Open AccessArticle
Anti-Neuroinflammatory Property of Phlorotannins from Ecklonia cava on Aβ25-35-Induced Damage in PC12 Cells
Mar. Drugs 2019, 17(1), 7; https://doi.org/10.3390/md17010007 - 22 Dec 2018
Cited by 2
Abstract
Alzheimer disease (AD) is a neurodegenerative disorder characterized by excessive accumulation of amyloid-beta peptide (Aβ) and progressive loss of neurons. Therefore, the inhibition of Aβ-induced neurotoxicity is a potential therapeutic approach for the treatment of AD. Ecklonia cava is an edible brown seaweed, [...] Read more.
Alzheimer disease (AD) is a neurodegenerative disorder characterized by excessive accumulation of amyloid-beta peptide (Aβ) and progressive loss of neurons. Therefore, the inhibition of Aβ-induced neurotoxicity is a potential therapeutic approach for the treatment of AD. Ecklonia cava is an edible brown seaweed, which has been recognized as a rich source of bioactive derivatives, mainly phlorotannins. In this study, phlorotannins including eckol, dieckol, 8,8′-bieckol were used as potential neuroprotective candidates for their anti-apoptotic and anti-inflammatory effects against Aβ25-35-induced damage in PC12 cells. Among the tested compounds, dieckol showed the highest effect in both suppressing intracellular oxidative stress and mitochondrial dysfunction and activation of caspase family. Three phlorotannins were found to inhibit TNF-α, IL-1β and PGE2 production at the protein levels. These result showed that the anti-inflammatory properties of our compounds are related to the down-regulation of proinflammatory enzymes, iNOS and COX-2, through the negative regulation of the NF-κB pathway in Aβ25-35-stimulated PC12 cells. Especially, dieckol showed the strong anti-inflammatory effects via suppression of p38, ERK and JNK. However, 8,8′-bieckol markedly decreased the phosphorylation of p38 and JNK and eckol suppressed the activation of p38. Therefore, the results of this study indicated that dieckol from E. cava might be applied as a drug candidate for the development of new generation therapeutic agents against AD. Full article
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Open AccessArticle
Open-Ring Butenolides from a Marine-Derived Anti-Neuroinflammatory Fungus Aspergillus terreus Y10
Mar. Drugs 2018, 16(11), 428; https://doi.org/10.3390/md16110428 - 02 Nov 2018
Cited by 2
Abstract
To investigate structurally novel and anti-neuroinflammatory natural compounds from marine-derived microorganisms, the secondary metabolites of Aspergillus terreus Y10, a fungus separated from the sediment of the coast in the South China Sea, were studied. Three new compounds (24), with [...] Read more.
To investigate structurally novel and anti-neuroinflammatory natural compounds from marine-derived microorganisms, the secondary metabolites of Aspergillus terreus Y10, a fungus separated from the sediment of the coast in the South China Sea, were studied. Three new compounds (24), with novel open-ring butenolide skeletons, were isolated from the ethyl acetate extract of the culture medium. In addition, a typical new butenolide, asperteretal F (1), was found to dose-dependently inhibit tumor necrosis factor (TNF-α) generation with an IC50 of 7.6 μg/mL. The present study shows the existence of open-ring butenolides, and suggests that butenolides such as asperteretal F (1) are a promising new anti-neuroinflammatroy candidate for neurodegenerative diseases. Full article
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Review

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Open AccessReview
Marine Compound Xyloketal B as a Potential Drug Development Target for Neuroprotection
Mar. Drugs 2018, 16(12), 516; https://doi.org/10.3390/md16120516 - 19 Dec 2018
Abstract
Xyloketal B is a natural compound isolated from the mangrove fungus, Xylaria sp. in the South China Sea. In the past decade, studies have shown that xyloketal B exhibits anti-oxidative, anti-inflammatory, and anti-apoptotic abilities and may serve as a treatment for ischemic stroke. [...] Read more.
Xyloketal B is a natural compound isolated from the mangrove fungus, Xylaria sp. in the South China Sea. In the past decade, studies have shown that xyloketal B exhibits anti-oxidative, anti-inflammatory, and anti-apoptotic abilities and may serve as a treatment for ischemic stroke. Xyloketal B has been shown to interact with both neurons and residential microglial cells and regulate a number of proteins involved in the apoptotic events during ischemia. Such mechanisms include inhibition of specific NADPH oxidase subunits, upregulation of HO-1, increase of Bcl-1/Bax ratio, and downregulation of TLR4 receptor. Both in vitro and in vivo stroke models have validated its potential in preventing ischemia-induced neuronal cell death. This review summarizes our current understanding of the effects of xyloketal B in ischemic conditions. As stroke ranks second in the causes of mortality worldwide and still lacks effective treatment, it is necessary to seek novel therapeutic options. Understanding the role of xyloketal B in ischemic stroke could reveal a new aspect of stroke treatment. Full article
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