Marine Bioactive Compounds with Potential Applications on Targets of CNS Associated with Neurodegenerative Disorders

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

Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 13150

Special Issue Editor

CNRS National Center for Disabled Scientific Research, Paris, France
Interests: neurotoxin discovery & characterization; mode of action of marine neurotoxins; nicotinic acetylcholine receptors; in-vitro electrophysiology; cyclic imine toxins; cyanobacterial neurotoxins; drug discovery & drug design; method development for neurotoxin detection
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Special Issue Information

Dear Colleagues,

Marine organisms are interesting sources of never-ending original bioactive compounds fueled by the emergence and on-going evolution of biosynthetic pathways in secondary metabolism and metabolic transformations in hosting organisms. As the population grows older, neurodegenerative disorders become the most important issue for public health. Marine bioactive compounds with potential applications on sensitive targets related to neurodegenerative disorders are the subject of this Special Issue of Marine Drugs. The pharmacological R&D for neurodegenerative diseases is highly developed, but the pharmacopeia is scarce given the multifactorial etiology of these neurodegenerative disorders. That is, of the four FDA-approved front-line drugs for the treatment of Alzheimer’s disease in 2017, three are acetylcholinesterase inhibitors, one inhibits NMDA receptors, and two act on α7 nicotinic acetylcholine receptors. This Special Issue will cover small alkaloids, polyketides to large peptides that even if not crossing the blood–brain barrier under normal conditions may constitute an alternative given their high affinities and easer bioengineering. Diverse marine sources of bioactive molecules ranging from picoplankton to green algae, from sponges, cnidarians, mollusks, to invertebrates and marine vertebrates, will be considered. Original articles and mini-reviews are welcome.

Dr. Romulo Aráoz
Guest Editor

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Keywords

  • marine natural products
  • drug discovery & mode of action
  • neurodegenerative diseases
  • cholinergic triad (nicotinic acetylcholine receptors, muscarinic acetylcholine receptors, acetylcholinesterase)
  • marine neurotoxins
  • marine neurotoxins directed against CNS targets involved in neurodegenerative diseases
  • neurotoxins from marine phytoplankton (dinoflagellates, diatoms, cyanobacteria)
  • secondary metabolites and neurodegenerative disorders

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Published Papers (2 papers)

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Research

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15 pages, 2740 KiB  
Article
Fucoidan Suppresses Mitochondrial Dysfunction and Cell Death against 1-Methyl-4-Phenylpyridinum-Induced Neuronal Cytotoxicity via Regulation of PGC-1α Expression
by Yong-Seok Han, Jun Hee Lee and Sang Hun Lee
Mar. Drugs 2019, 17(9), 518; https://doi.org/10.3390/md17090518 - 2 Sep 2019
Cited by 16 | Viewed by 4124
Abstract
Mitochondria are considered to be the powerhouses of cells. They are the most commonly damaged organelles within dopaminergic neurons in patients with Parkinson’s disease (PD). Despite the importance of protecting neuronal mitochondria in PD patients, the detailed mechanisms underlying mitochondrial dysfunction during pathogenesis [...] Read more.
Mitochondria are considered to be the powerhouses of cells. They are the most commonly damaged organelles within dopaminergic neurons in patients with Parkinson’s disease (PD). Despite the importance of protecting neuronal mitochondria in PD patients, the detailed mechanisms underlying mitochondrial dysfunction during pathogenesis and pathophysiological progression of PD have not yet been elucidated. We investigated the protective action of fucoidan against the detrimental action of 1-methyl-4-phenyl-pyridinium (MPP+), a neurotoxin used to model PD, in the mitochondria of SH-SY5Y neural cells. Fucoidan increased the expression of peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) and protected the cells from MPP+-induced apoptosis by upregulating the 5′ adenosine monophosphate-activated protein kinase (AMPK)-PGC-1α axis. These effects were blocked by the silencing of the PGC-1α axis. These results indicated that fucoidan protects SH-SY5Y cells from mitochondrial dysfunction and cell death caused by MPP+ treatment, via the AMPK-PGC-1α axis. These findings also suggest that fucoidan could potentially be used as a therapeutic agent for PD. Full article
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Review

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20 pages, 2662 KiB  
Review
Marine-Derived Natural Compounds for the Treatment of Parkinson’s Disease
by Chunhui Huang, Zaijun Zhang and Wei Cui
Mar. Drugs 2019, 17(4), 221; https://doi.org/10.3390/md17040221 - 11 Apr 2019
Cited by 36 | Viewed by 8240
Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder caused by the loss of dopaminergic neurons, leading to the motor dysfunctions of patients. Although the etiology of PD is still unclear, the death of dopaminergic neurons during PD progress was revealed to be associated with [...] Read more.
Parkinson’s disease (PD) is a neurodegenerative disorder caused by the loss of dopaminergic neurons, leading to the motor dysfunctions of patients. Although the etiology of PD is still unclear, the death of dopaminergic neurons during PD progress was revealed to be associated with the abnormal aggregation of α-synuclein, the elevation of oxidative stress, the dysfunction of mitochondrial functions, and the increase of neuroinflammation. However, current anti-PD therapies could only produce symptom-relieving effects, because they could not provide neuroprotective effects, stop or delay the degeneration of dopaminergic neurons. Marine-derived natural compounds, with their novel chemical structures and unique biological activities, may provide anti-PD neuroprotective effects. In this study, we have summarized anti-PD marine-derived natural products which have shown pharmacological activities by acting on various PD targets, such as α-synuclein, monoamine oxidase B, and reactive oxygen species. Moreover, marine-derived natural compounds currently evaluated in the clinical trials for the treatment of PD are also discussed. Full article
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