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Neuroprotective Agents II
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Neuroprotective Agents II

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

Deadline for manuscript submissions: 31 May 2024 | Viewed by 10400

Special Issue Editor

Prof. Dr. Jia Zhou

E-Mail Website1 Website2
Guest Editor
Chemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX 77555, USA
Interests: drug discovery and development; 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 Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroprotection represents one of the most appealing therapeutic strategies for preventing neurodegeneration and mitigating neuronal damage. The development of novel neuroprotective agents has attracted tremendous drug discovery efforts, which aim to identify 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 the earlier Molecules Special Issue “Neuroprotective Agents”. I hope that issue will continue to 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. Due to the wide interest in that first edition of the Molecules Special Issue, we have decided to continue the consideration of neuroprotective agents and related topics. We are therefore looking forward to gathering submissions and presenting further advances in the second edition of this Special Issue, entitled “Neuroprotective Agents II”.

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 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. Molecules is an international peer-reviewed open access semimonthly 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 2700 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 (3 papers)

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Research

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31 pages, 11901 KiB  
Article
Activation of IGF-1/GLP-1 Signalling via 4-Hydroxyisoleucine Prevents Motor Neuron Impairments in Experimental ALS-Rats Exposed to Methylmercury-Induced Neurotoxicity
by Ambika Shandilya, Sidharth Mehan, Sumit Kumar, Pranshul Sethi, Acharan S. Narula, Abdulrahman Alshammari, Metab Alharbi and Abdullah F. Alasmari
Molecules 2022, 27(12), 3878; https://doi.org/10.3390/molecules27123878 - 16 Jun 2022
Cited by 17 | Viewed by 3140
Abstract
Amyotrophic lateral sclerosis (ALS) is a severe adult motor neuron disease that causes progressive neuromuscular atrophy, muscle wasting, weakness, and depressive-like symptoms. Our previous research suggests that mercury levels are directly associated with ALS progression. MeHg+-induced ALS is characterised by oligodendrocyte destruction, myelin [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a severe adult motor neuron disease that causes progressive neuromuscular atrophy, muscle wasting, weakness, and depressive-like symptoms. Our previous research suggests that mercury levels are directly associated with ALS progression. MeHg+-induced ALS is characterised by oligodendrocyte destruction, myelin basic protein (MBP) depletion, and white matter degeneration, leading to demyelination and motor neuron death. The selection of MeHg+ as a potential neurotoxicant is based on our evidence that it has been connected to the development of ALS-like characteristics. It causes glutamate-mediated excitotoxicity, calcium-dependent neurotoxicity, and an ALS-like phenotype. Dysregulation of IGF-1/GLP-1 signalling has been associated with ALS progression. The bioactive amino acid 4-hydroxyisoleucine (HI) from Trigonella foenum graecum acts as an insulin mimic in rodents and increases insulin sensitivity. This study examined the neuroprotective effects of 4-HI on MeHg+-treated adult Wistar rats with ALS-like symptoms, emphasising brain IGF1/GLP-1 activation. Furthermore, we investigated the effect of 4-HI on MBP levels in rat brain homogenate, cerebrospinal fluid (CSF), blood plasma, and cell death indicators such as caspase-3, Bax, and Bcl-2. Rats were assessed for muscular strength, locomotor deficits, depressed behaviour, and spatial learning in the Morris water maze (MWM) to measure neurobehavioral abnormalities. Doses of 4-HI were given orally for 42 days in the MeHg+ rat model at 50 mg/kg or 100 mg/kg to ameliorate ALS-like neurological dysfunctions. Additionally, neurotransmitters and oxidative stress markers were examined in rat brain homogenates. Our findings suggest that 4-HI has neuroprotective benefits in reducing MeHg+-induced behavioural, neurochemical, and histopathological abnormalities in ALS-like rats exposed to methylmercury. Full article
(This article belongs to the Special Issue Neuroprotective Agents II)
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Review

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29 pages, 5138 KiB  
Review
A New Therapeutic Trend: Natural Medicine for Ameliorating Ischemic Stroke via PI3K/Akt Signaling Pathway
by Xian Liu, Xinyu Xiao, Xue Han, Lan Yao and Wei Lan
Molecules 2022, 27(22), 7963; https://doi.org/10.3390/molecules27227963 - 17 Nov 2022
Cited by 13 | Viewed by 3197
Abstract
Ischemic stroke (IS) is an acute cerebrovascular disease caused by sudden arterial occlusion, which is characterized by a high morbidity, mortality, and disability rate. It is one of the most important causes of nervous system morbidity and mortality in the world. In recent [...] Read more.
Ischemic stroke (IS) is an acute cerebrovascular disease caused by sudden arterial occlusion, which is characterized by a high morbidity, mortality, and disability rate. It is one of the most important causes of nervous system morbidity and mortality in the world. In recent years, the search for new medicine for the treatment of IS has become an attractive research focus. Due to the extremely limited time window of traditional medicine treatment, some side effects may occur, and accompanied by the occurrence of adverse reactions, the frequency of exploration with natural medicine is significantly increased. Phosphatidylinositol-3-kinase/Protein kinase B (PI3K/Akt) signaling pathway is a classical pathway for cell metabolism, growth, apoptosis, and other physiological activities. There is considerable research on medicine that treats various diseases through this pathway. This review focuses on how natural medicines (including herbs and insects) regulate important pathophysiological processes such as inflammation, oxidative stress, apoptosis, and autophagy through the PI3K/Akt signaling pathway, and the role it plays in improving IS. We found that many kinds of herbal medicine and insect medicine can alleviate the damage caused by IS through the PI3K/Akt signaling pathway. Moreover, the prescription after their combination can also achieve certain results. Therefore, this review provides a new candidate category for medicine development in the treatment of IS. Full article
(This article belongs to the Special Issue Neuroprotective Agents II)
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16 pages, 633 KiB  
Review
Mechanism and Regulation of Microglia Polarization in Intracerebral Hemorrhage
by Yuting Guo, Weibo Dai, Yan Zheng, Weilin Qiao, Weixuan Chen, Lihua Peng, Hua Zhou, Tingting Zhao, Huimin Liu, Feng Zheng and Peng Sun
Molecules 2022, 27(20), 7080; https://doi.org/10.3390/molecules27207080 - 20 Oct 2022
Cited by 8 | Viewed by 3205
Abstract
Intracerebral hemorrhage (ICH) is the most lethal subtype of stroke, but effective treatments are lacking, and neuroinflammation plays a key role in the pathogenesis. In the innate immune response to cerebral hemorrhage, microglia first appear around the injured tissue and are involved in [...] Read more.
Intracerebral hemorrhage (ICH) is the most lethal subtype of stroke, but effective treatments are lacking, and neuroinflammation plays a key role in the pathogenesis. In the innate immune response to cerebral hemorrhage, microglia first appear around the injured tissue and are involved in the inflammatory cascade response. Microglia respond to acute brain injury by being activated and polarized to either a typical M1-like (pro-inflammatory) or an alternative M2-like (anti-inflammatory) phenotype. These two polarization states produce pro-inflammatory or anti-inflammatory. With the discovery of the molecular mechanisms and key signaling molecules related to the polarization of microglia in the brain, some targets that regulate the polarization of microglia to reduce the inflammatory response are considered a treatment for secondary brain tissue after ICH damage effective strategies. Therefore, how to promote the polarization of microglia to the M2 phenotype after ICH has become the focus of attention in recent years. This article reviews the mechanism of action of microglia’s M1 and M2 phenotypes in secondary brain injury after ICH. Moreover, it discusses compounds and natural pharmaceutical ingredients that can polarize the M1 to the M2 phenotype. Full article
(This article belongs to the Special Issue Neuroprotective Agents II)
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