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Special Issue "Neuroprotective Agents"

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: 30 December 2017

Special Issue Editor

Guest Editor
Prof. Dr. Jia Zhou

Chemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX 77555, USA
Website1 | Website2 | E-Mail
Interests: drug discovery; target-based drug design; fragment/structure-based drug design; pharmacological tools; CNS therapeutics; neuroprotective agents; anticancer agents; anti-inflammatory agents; antiviral agents; drug development; chemical biology

Special Issue Information

Dear Colleagues,

Neuroprotection represents one of the most appealing therapeutic strategies for preventing neurodegeneration and mitigating against neuronal damage.  The development of novel neuroprotective agents has attracted tremendous drug discovery efforts, with the aim of identifying effective neurotherapeutics for a variety of central nervous system (CNS) disorders, including neurodegenerative diseases such as Alzheimer's disease (AD),  Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), dementia, stroke, traumatic brain injury (TBI), spinal cord injury, schizophrenia, drug abuse-induced neurotoxicity (i.e. methamphetamine overdoses), and even retinal diseases and glaucoma. This Special Issue aims to provide a forum for the dissemination of the latest information on new molecules including both synthetic compounds and natural products as well as novel drug targets associated with neuroprotective agents. As the Guest Editor, I would like to thank all the authors for their tremendous effort, dedication, and excellent contribution to this special issue of Neuroprotective Agents. I hope that this issue will serve as a key reference work for medicinal chemists, chemical biologists, neuropharmacologists, and other research investigators engaged in or interested in neuroprotection and neuroprotective agent drug discovery and development.

Prof. Dr. Jia Zhou
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 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. Molecules 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

  • neuroprotection
  • neuroprotective agents
  • neuroprotective drugs
  • neurotherapeutics
  • neuroapoptosis
  • neuronal cell death
  • drug discovery and development
  • synthetic molecules
  • natural products
  • drug targets and mechanisms
  • central nervous system (CNS) disorders
  • neurodegenerative diseases
  • Alzheimer's disease (AD)
  • Parkinson's disease (PD)
  • amyotrophic lateral sclerosis (ALS)
  • dementia
  • stroke
  • traumatic brain injury (TBI)
  • spinal cord injury
  • schizophrenia
  • drug abuse-induced neurotoxicity (i.e. methamphetamine overdoses)
  • retinal diseases and glaucoma

Published Papers (4 papers)

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Research

Open AccessArticle α-Synuclein Regulates Neuronal Cholesterol Efflux
Molecules 2017, 22(10), 1769; doi:10.3390/molecules22101769
Received: 26 September 2017 / Revised: 18 October 2017 / Accepted: 19 October 2017 / Published: 19 October 2017
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Abstract
α-Synuclein is a neuronal protein that is at the center of focus in understanding the etiology of a group of neurodegenerative diseases called α-synucleinopathies, which includes Parkinson’s disease (PD). Despite much research, the exact physiological function of α-synuclein is still unclear. α-Synuclein has
[...] Read more.
α-Synuclein is a neuronal protein that is at the center of focus in understanding the etiology of a group of neurodegenerative diseases called α-synucleinopathies, which includes Parkinson’s disease (PD). Despite much research, the exact physiological function of α-synuclein is still unclear. α-Synuclein has similar biophysical properties as apolipoproteins and other lipid-binding proteins and has a high affinity for cholesterol. These properties suggest a possible role for α-synuclein as a lipid acceptor mediating cholesterol efflux (the process of removing cholesterol out of cells). To test this concept, we “loaded” SK-N-SH neuronal cells with fluorescently-labelled cholesterol, applied exogenous α-synuclein, and measured the amount of cholesterol removed from the cells using a classic cholesterol efflux assay. We found that α-synuclein potently stimulated cholesterol efflux. We found that the process was dose and time dependent, and was saturable at 1.0 µg/mL of α-synuclein. It was also dependent on the transporter protein ABCA1 located on the plasma membrane. We reveal for the first time a novel role of α-synuclein that underscores its importance in neuronal cholesterol regulation, and identify novel therapeutic targets for controlling cellular cholesterol levels. Full article
(This article belongs to the Special Issue Neuroprotective Agents)
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Figure 1

Open AccessArticle Ginsenoside Rg3 Prevents Oxidative Stress-Induced Astrocytic Senescence and Ameliorates Senescence Paracrine Effects on Glioblastoma
Molecules 2017, 22(9), 1516; doi:10.3390/molecules22091516
Received: 1 August 2017 / Revised: 22 August 2017 / Accepted: 8 September 2017 / Published: 10 September 2017
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Abstract
Senescent astrocytes in aging brain express senescence-associated secretory phenotype (SASP) and link with increased brain aging and its related diseases. In order to determine whether ginsenosides ameliorate the astrocytic senescence in vitro, human astrocytic CRT cells and primary rat astrocytes were used in
[...] Read more.
Senescent astrocytes in aging brain express senescence-associated secretory phenotype (SASP) and link with increased brain aging and its related diseases. In order to determine whether ginsenosides ameliorate the astrocytic senescence in vitro, human astrocytic CRT cells and primary rat astrocytes were used in the present study. Ginsenosides Rg1, Re, Rb1 and Rg3 (5 μg/mL) could effectively prevent the astrocytic senescence induced by H2O2 exposure. However, these ginsenosides did not reverse the astrocytic senescence. Importantly, senescent astrocytes herein produce SASP. The expression of major components of SASP, IL-6 and IL-8, are greatly increased in senescent astrocytes. Ginsenoside Rg3 (10 μg/mL) effectively suppressed the expressions of IL-6 and IL-8, which is associated with regulations of NF-κB and p38MAPK activation. In addition, after incubation with Rg3, conditioned medium from senescent astrocytic CRT cells significantly decreased the ability to promote the proliferation of astrocytoma U373-MG, U87-MG and U251-MG cells compared with non-treated senescent samples. Similar patterns were confirmed in chemotherapy-induced glioblastoma senescent cells. The present study explored a potential candidate for amelioration of astrocytic senescence and SASP in brain aging, which provided a basis for developing strategies to reduce the dark side of senescence in normal or pathological aging process. Full article
(This article belongs to the Special Issue Neuroprotective Agents)
Figures

Open AccessArticle Trehalose Inhibits A53T Mutant α-Synuclein Overexpression and Neurotoxicity in Transduced PC12 Cells
Molecules 2017, 22(8), 1293; doi:10.3390/molecules22081293
Received: 6 July 2017 / Accepted: 1 August 2017 / Published: 8 August 2017
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Abstract
Fibrillar accumulation of A53T mutant α-synuclein (A53T-AS) in Lewy bodies is a symptom of Parkinsonism. Inhibitions of the overexpression and fibrillar aggregation of α-synuclein (AS) in vivo could be a promising strategy for treating Parkinson’s disease (PD). In this study, at concentrations lower
[...] Read more.
Fibrillar accumulation of A53T mutant α-synuclein (A53T-AS) in Lewy bodies is a symptom of Parkinsonism. Inhibitions of the overexpression and fibrillar aggregation of α-synuclein (AS) in vivo could be a promising strategy for treating Parkinson’s disease (PD). In this study, at concentrations lower than 1 mM, trehalose decreased the A53T-AS expression level in transduced PC12 cells. Although H2O2 and aluminum ions increased the expression level and neurotoxicity of A53T-AS in cells, proper trehalose concentrations inhibited the event. These studies adequately prove that trehalose at an appropriate dose would be potentially useful for PD treatment. Full article
(This article belongs to the Special Issue Neuroprotective Agents)
Figures

Open AccessArticle Effects of P-Glycoprotein on the Transport of DL0410, a Potential Multifunctional Anti-Alzheimer Agent
Molecules 2017, 22(8), 1246; doi:10.3390/molecules22081246
Received: 5 July 2017 / Revised: 17 July 2017 / Accepted: 23 July 2017 / Published: 25 July 2017
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Abstract
In our study, we attempted to investigate the influences of P-glycoprotein (P-gp) on DL0410, a novel synthetic molecule for Alzheimer’s disease (AD) treatment, for intestinal absorption and blood-brain barrier permeability in vitro and related binding mechanisms in silico. Caco-2, MDCK, and MDCK-MDR1 cells
[...] Read more.
In our study, we attempted to investigate the influences of P-glycoprotein (P-gp) on DL0410, a novel synthetic molecule for Alzheimer’s disease (AD) treatment, for intestinal absorption and blood-brain barrier permeability in vitro and related binding mechanisms in silico. Caco-2, MDCK, and MDCK-MDR1 cells were utilized for transport studies, and homology modelling of human P-gp was built for further docking study to uncover the binding mode of DL0410. The results showed that the apparent permeability (Papp) value of DL0410 was approximately 1 × 10−6 cm/s, indicating the low permeability of DL0410. With the presence of verapamil, the directional transport of DL0410 disappeared in Caco-2 and MDCK-MDR1 cells, suggesting that DL0410 should be a substrate of P-gp, which was also confirmed by P-gp ATPase assay. In addition, DL0410 could competitively inhibit the transport of Rho123, a P-gp known substrate. According to molecular docking, we also found that DL0410 could bind to the drug binding pocket (DBP), but not the nucleotide binding domain (NBD). In conclusion, DL0410 was a substrate as well as a competitive inhibitor of P-gp, and P-gp had a remarkable impact on the intestine and brain permeability of DL0410, which is of significance for drug research and development. Full article
(This article belongs to the Special Issue Neuroprotective Agents)
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