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Special Issue "Marine Compounds in Neurodegenerative Diseases"

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

Deadline for manuscript submissions: closed (24 August 2018)

Special Issue Editors

Guest Editor
Prof. Dr. Patrizia Russo

IRCCS San Raffaele Pisana, Area of Clinical and Molecular Epidemiology, 00166 Rome, Italy
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Interests: Applied biology,nicotinic receptor in cancer, COPD, addiction, Alzheimer, systems medicine
Guest Editor
Prof. Dr. Massimo Fini

Scientific Direction, IRCCS San Raffaele Pisana, Rome, Italy
E-Mail
Phone: 06-6613-0405
Interests: Systems medicine, aging, frailty, rehabilitation, cardiovascular

Special Issue Information

Dear Colleagues,

Aging-associated neurodegenerative diseases (NDs), such as Alzheimer's disease (AD) and AD-like pathologies, such as changes in Aβ40/42 ratios, tau hyperphosphorylation and endosome abnormalities, Parkinson's disease (PD), frontotemporal degeneration (FTD) and amyotrophic lateral sclerosis (ALS), among others, are unremittingly progressive and fatal neurological diseases. NDs are characterized by irreversible loss of neurons/cholinergic or dopaminergic receptors functionality that results in apoptosis and, in turn, in severe atrophy of the affected patient brain regions. Pathogenesis of NDs are complex and the underlying mechanisms are yet to be fully explored.

Neurodegeneration is associated to neuroinflammation a dynamic biological response characterized by the recruitment of innate and adaptive immune system cells in the site of tissue damage. Activation of resident microglia and infiltrating immune cells may contribute to the disease process itself.

This Special Issue “Marine Compounds in Neurodegenerative Diseases” of Marine Drugs will cover the whole scope of agents targeting the mechanisms underlying NDs. This Special issue is focused on (but not limited to) compounds with relevant biological activities; however, preclinical drugs are also investigated.

Prof. Dr. Patrizia Russo
Prof. Dr. Massimo Fini
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 1800 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

  • neurodegenerative diseases
  • neuroinflammation
  • marine compounds
  • cell death
  • cell survival
  • drug resistance
  • necrosis

Published Papers (6 papers)

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Research

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Open AccessArticle Fucosterol from an Edible Brown Alga Ecklonia stolonifera Prevents Soluble Amyloid Beta-Induced Cognitive Dysfunction in Aging Rats
Mar. Drugs 2018, 16(10), 368; https://doi.org/10.3390/md16100368
Received: 3 September 2018 / Revised: 26 September 2018 / Accepted: 3 October 2018 / Published: 5 October 2018
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Abstract
Fucosterol from edible brown seaweeds has various biological activities, including anti-inflammatory, anti-adipogenic, antiphotoaging, anti-acetylcholinesterase, and anti-beta-secretase 1 activities. However, little is known about its effects on soluble amyloid beta peptide (sAβ)-induced endoplasmic reticulum (ER) stress and cognitive impairment. Fucosterol was isolated from the
[...] Read more.
Fucosterol from edible brown seaweeds has various biological activities, including anti-inflammatory, anti-adipogenic, antiphotoaging, anti-acetylcholinesterase, and anti-beta-secretase 1 activities. However, little is known about its effects on soluble amyloid beta peptide (sAβ)-induced endoplasmic reticulum (ER) stress and cognitive impairment. Fucosterol was isolated from the edible brown seaweed Ecklonia stolonifera, and its neuroprotective effects were analyzed in primary hippocampal neurons and in aging rats. Fucosterol attenuated sAβ1-42-induced decrease in the viability of hippocampal neurons and downregulated sAβ1-42-induced increase in glucose-regulated protein 78 (GRP78) expression in hippocampal neurons via activation of tyrosine receptor kinase B-mediated ERK1/2 signaling. Fucosterol co-infusion attenuated sAβ1-42-induced cognitive impairment in aging rats via downregulation of GRP78 expression and upregulation of mature brain-derived neurotrophic factor expression in the dentate gyrus. Fucosterol might be beneficial for the management of cognitive dysfunction via suppression of aging-induced ER stress. Full article
(This article belongs to the Special Issue Marine Compounds in Neurodegenerative Diseases)
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Open AccessArticle The Protective Effects of Clams on Hypercholesterolemia in Late-Stage Triple-Transgenic Alzheimer’s Diseased Mice Hearts
Mar. Drugs 2018, 16(8), 263; https://doi.org/10.3390/md16080263
Received: 22 June 2018 / Revised: 18 July 2018 / Accepted: 28 July 2018 / Published: 1 August 2018
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Abstract
To investigate a high cholesterol diet in Alzheimer’s disease (AD) mice, they were fed with (2% cholesterol) in five groups with a control group, AD mice group, AD mice plus Meretrix lusoria group, AD mice plus Geloina eros group, and, AD mice plus
[...] Read more.
To investigate a high cholesterol diet in Alzheimer’s disease (AD) mice, they were fed with (2% cholesterol) in five groups with a control group, AD mice group, AD mice plus Meretrix lusoria group, AD mice plus Geloina eros group, and, AD mice plus Corbicula fluminea group for three months, and treated with the fatty acid profiles of clams by gas chromatography (GC). The results showed that treatment with clams for three months reduced Fas/L and Caspase-3 in the Meretrix lusoria and Geloina eros groups, but Fas-associated death domain (FADD) and Caspase-8 were strongly reduced in the Geloina eros group. For the mitochondria-dependent apoptotic pathway, the reduction of apoptosis proteins were observed in the hearts of clams-treated AD mice. BAK and Caspase-9 was reduced in the Meretrix lusoria group, but Caspase-3 and Cytochrome-c were reduced in Geloina eros group. Enhancement of survival proteins p-AKT, p-IGF1R, p-PI3K, Bcl-XL, Bcl2, and the longevity SIRT1 signaling proteins, p-AMPK-α, SIRT1, PGC1-α, p-FOXO3 were observed in clams-treated mice and even more strongly enhanced in the Meretrix lusoria, Geloina eros and Corbicula fluminea groups. This study observed that the ingestion of clams caused a reduction of apoptosis proteins and enhancement of survival and SIRT1 signaling proteins in the hearts. Full article
(This article belongs to the Special Issue Marine Compounds in Neurodegenerative Diseases)
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Open AccessArticle Oligo-Porphyran Ameliorates Neurobehavioral Deficits in Parkinsonian Mice by Regulating the PI3K/Akt/Bcl-2 Pathway
Mar. Drugs 2018, 16(3), 82; https://doi.org/10.3390/md16030082
Received: 3 January 2018 / Revised: 21 February 2018 / Accepted: 2 March 2018 / Published: 6 March 2018
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Abstract
Parkinson’s disease (PD) is a neurodegenerative movement disorder that is caused by a selective loss of dopaminergic neurons. Current PD treatments provide symptomatic relief but do not prevent or decelerate disease progression. Previous studies have suggested that acetylated and phosphorylated porphyran, derived from
[...] Read more.
Parkinson’s disease (PD) is a neurodegenerative movement disorder that is caused by a selective loss of dopaminergic neurons. Current PD treatments provide symptomatic relief but do not prevent or decelerate disease progression. Previous studies have suggested that acetylated and phosphorylated porphyran, derived from Porphyra, produces a neuroprotective effect against 6-OHDA-induced damage. Due to its antioxidant and neuroprotective potential, this study evaluates whether oligo-porphyran (OP) could be beneficial in an experimental model of PD in mice. The drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was intraperitoneally injected (20 mg/kg body weight) for seven days to simulate PD, followed by OP administration. We found that the behavioral deficits in spontaneous motor activity, latency to descend in a pole test, and suspension in a traction test were ameliorated, and excessive dopamine (DA) metabolism was suppressed after OP treatment. Additionally, we found that OP protected dopaminergic neurons by preventing MPTP-induced decreases in dopaminergic transporter and tyrosine hydroxylase protein levels. We speculated whether OP regulates a signaling pathway that affects the behavioral changes seen in PD mice. In this study, the PI3K/Akt/Bcl-2 pathway was detected. Our results demonstrate that OP increased the phosphorylation of PI3K/Akt/GSK-3β and inhibited the activation of caspase-3 and poly (ADP-ribose) polymerase, with changes in the Bax/Bcl-2 ratio. These results showed that OP might promote DA neuron survival in vivo by regulating the PI3K/Akt/Bcl-2 pathway, thereby ameliorating the neurobehavioral deficits in a PD mouse model and suggesting OP as a neuroprotective treatment for PD. Full article
(This article belongs to the Special Issue Marine Compounds in Neurodegenerative Diseases)
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Review

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Open AccessReview Cognitive Impairment in Chronic Obstructive Pulmonary Disease (COPD): Possible Utility of Marine Bioactive Compounds
Mar. Drugs 2018, 16(9), 313; https://doi.org/10.3390/md16090313
Received: 16 July 2018 / Revised: 30 August 2018 / Accepted: 30 August 2018 / Published: 4 September 2018
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Abstract
Chronic obstructive pulmonary disease (COPD) is characterized by long-term airflow limitation. Early-onset COPD in non-smoker subjects is ≥60 years and in the elderly is often associated with different comorbidities. Cognitive impairment is one of the most common feature in patients with COPD, and
[...] Read more.
Chronic obstructive pulmonary disease (COPD) is characterized by long-term airflow limitation. Early-onset COPD in non-smoker subjects is ≥60 years and in the elderly is often associated with different comorbidities. Cognitive impairment is one of the most common feature in patients with COPD, and is associated with COPD severity and comorbidities. Cognitive impairment in COPD enhances the assistance requirement in different aspects of daily living, treatment adherence, and effectual self-management.This review describes various bioactive compounds of natural marine sources that modulate different targets shared by both COPD and cognitive impairment and hypothesizes a possible link between these two syndromes. Full article
(This article belongs to the Special Issue Marine Compounds in Neurodegenerative Diseases)
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Open AccessReview On the Neuroprotective Role of Astaxanthin: New Perspectives?
Mar. Drugs 2018, 16(8), 247; https://doi.org/10.3390/md16080247
Received: 11 July 2018 / Revised: 20 July 2018 / Accepted: 23 July 2018 / Published: 24 July 2018
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Abstract
Astaxanthin is a carotenoid with powerful antioxidant and anti-inflammatory activity produced by several freshwater and marine microorganisms, including bacteria, yeast, fungi, and microalgae. Due to its deep red-orange color it confers a reddish hue to the flesh of salmon, shrimps, lobsters, and crayfish
[...] Read more.
Astaxanthin is a carotenoid with powerful antioxidant and anti-inflammatory activity produced by several freshwater and marine microorganisms, including bacteria, yeast, fungi, and microalgae. Due to its deep red-orange color it confers a reddish hue to the flesh of salmon, shrimps, lobsters, and crayfish that feed on astaxanthin-producing organisms, which helps protect their immune system and increase their fertility. From the nutritional point of view, astaxanthin is considered one of the strongest antioxidants in nature, due to its high scavenging potential of free radicals in the human body. Recently, astaxanthin is also receiving attention for its effect on the prevention or co-treatment of neurological pathologies, including Alzheimer and Parkinson diseases. In this review, we focus on the neuroprotective properties of astaxanthin and explore the underlying mechanisms to counteract neurological diseases, mainly based on its capability to cross the blood-brain barrier and its oxidative, anti-inflammatory, and anti-apoptotic properties. Full article
(This article belongs to the Special Issue Marine Compounds in Neurodegenerative Diseases)
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Open AccessReview Application of Chitosan, Chitooligosaccharide, and Their Derivatives in the Treatment of Alzheimer’s Disease
Mar. Drugs 2017, 15(11), 322; https://doi.org/10.3390/md15110322
Received: 23 September 2017 / Revised: 12 October 2017 / Accepted: 13 October 2017 / Published: 7 November 2017
Cited by 3 | PDF Full-text (421 KB) | HTML Full-text | XML Full-text
Abstract
Classic hypotheses of Alzheimer’s disease (AD) include cholinergic neuron death, acetylcholine (ACh) deficiency, metal ion dynamic equilibrium disorder, and deposition of amyloid and tau. Increased evidence suggests neuroinflammation and oxidative stress may cause AD. However, none of these factors induces AD independently, but
[...] Read more.
Classic hypotheses of Alzheimer’s disease (AD) include cholinergic neuron death, acetylcholine (ACh) deficiency, metal ion dynamic equilibrium disorder, and deposition of amyloid and tau. Increased evidence suggests neuroinflammation and oxidative stress may cause AD. However, none of these factors induces AD independently, but they are all associated with the formation of Aβ and tau proteins. Current clinical treatments based on ACh deficiency can only temporarily relieve symptoms, accompanied with many side-effects. Hence, searching for natural neuroprotective agents, which can significantly improve the major symptoms and reverse disease progress, have received great attention. Currently, several bioactive marine products have shown neuroprotective activities, immunomodulatory and anti-inflammatory effects with low toxicity and mild side effects in laboratory studies. Recently, chitosan (CTS), chitooligosaccharide (COS) and their derivatives from exoskeletons of crustaceans and cell walls of fungi have shown neuroprotective and antioxidative effects, matrix metalloproteinase inhibition, anti-HIV and anti-inflammatory properties. With regards to the hypotheses of AD, the neuroprotective effect of CTS, COS, and their derivatives on AD-like changes in several models have been reported. CTS and COS exert beneficial effects on cognitive impairments via inhibiting oxidative stress and neuroinflammation. They are also a new type of non-toxic β-secretase and AChE inhibitor. As neuroprotective agents, they could reduce the cell membrane damage caused by copper ions and decrease the content of reactive oxygen species. This review will focus on their anti-neuroinflammation, antioxidants and their inhibition of β-amyloid, acetylcholinesterase and copper ions adsorption. Finally, the limitations and future work will be discussed. Full article
(This article belongs to the Special Issue Marine Compounds in Neurodegenerative Diseases)
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