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Chemical Agents for Neurodegenerative Diseases
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Chemical Agents for Neurodegenerative Diseases

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

Deadline for manuscript submissions: closed (20 January 2024) | Viewed by 8389

Special Issue Editor

Prof. Dr. Nan Gao

E-Mail Website
Guest Editor
Key Laboratory of Polyoxometalate and Reticular Material Chemistry of Ministry of Education and Faculty of Chemistry, Northeast Normal University, Changchun, China
Interests: Alzheimer's disease; porous aromatic frameworks; chemical agents; polyoxometalates; nanomaterials

Special Issue Information

Dear Colleagues,

In modern society, human life expectancy is increasing, while birth rates are decreasing. Therefore, the trend of population aging is inevitable, and the above problems have also led to more patients with neurodegenerative diseases, which poses a severe challenge to national health care systems and the economic security of families. Common neurodegenerative diseases mainly include Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS) and so on. In recent years, therapeutic agents for neurodegenerative diseases based on small molecules, polymers and nanomaterials have shown excellent diagnostic and therapeutic properties. We hope that with the help of this Special Issue we can further promote the application of chemical agents in neurodegenerative diseases.

Prof. Dr. Nan Gao
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

  • neurodegenerative diseases
  • chemical agents
  • small molecules
  • polymers
  • nanomaterials

Published Papers (3 papers)

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Research

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17 pages, 3637 KiB  
Article
Sigma-1 Receptor Activation Improves Oligodendrogenesis and Promotes White-Matter Integrity after Stroke in Mice with Diabetic Mellitus
by Wenjing Song, Yang Yao, Heling Zhang, Xin Hao, Liping Zhou, Zhixiao Song, Tiantian Wei, Tianyan Chi, Peng Liu, Xuefei Ji and Libo Zou
Molecules 2023, 28(1), 390; https://doi.org/10.3390/molecules28010390 - 02 Jan 2023
Cited by 1 | Viewed by 2135
Abstract
Diabetes mellitus (DM) is a major risk factor for stroke and exacerbates white-matter damage in focal cerebral ischemia. Our previous study showed that the sigma-1 receptor agonist PRE084 ameliorates bilateral common-carotid-artery occlusion-induced brain damage in mice. However, whether this protective effect can extend [...] Read more.
Diabetes mellitus (DM) is a major risk factor for stroke and exacerbates white-matter damage in focal cerebral ischemia. Our previous study showed that the sigma-1 receptor agonist PRE084 ameliorates bilateral common-carotid-artery occlusion-induced brain damage in mice. However, whether this protective effect can extend to white matter remains unclear. In this study, C57BL/6 mice were treated with high-fat diets (HFDs) combined with streptozotocin (STZ) injection to mimic type 2 diabetes mellitus (T2DM). Focal cerebral ischemia in T2DM mice was established via injection of the vasoconstrictor peptide endothelin-1 (ET-1) into the hippocampus. Three different treatment plans were used in this study. In one plan, 1 mg/kg of PRE084 (intraperitoneally) was administered for 7 d before ET-1 injection; the mice were sacrificed 24 h after ET-1 injection. In another plan, PRE084 treatment was initiated 24 h after ET-1 injection and lasted for 7 d. In the third plan, PRE084 treatment was initiated 24 h after ET-1 injection and lasted for 21 d. The Y-maze, novel object recognition, and passive avoidance tests were used to assess neurobehavioral outcomes. We found no cognitive dysfunction or white-matter damage 24 h after ET-1 injection. However, 7 and 21 d after ET-1 injection, the mice showed significant cognitive impairment and white-matter damage. Only PRE084 treatment for 21 d could improve this white-matter injury; increase axon and myelin density; decrease demyelination; and increase the expressions of myelin regulator 2‘-3‘-cyclic nucleotide 3‘-phosphodiesterase (CNpase) and myelin oligodendrocyte protein (MOG) (which was expressed by mature oligodendrocytes), the number of nerve/glial-antigen 2 (NG2)-positive cells, and the expression of platelet-derived growth factor receptor-alpha (PDGFRα), all of which were expressed by oligodendrocyte progenitor cells in mice with diabetes and focal cerebral ischemia. These results indicate that maybe there was more severe white-matter damage in the focal cerebral ischemia of the diabetic mice than in the mice with normal blood glucose levels. Long-term sigma-1 receptor activation may promote oligodendrogenesis and white-matter functional recovery in patients with stroke and with diabetes. Full article
(This article belongs to the Special Issue Chemical Agents for Neurodegenerative Diseases)
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Review

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38 pages, 3589 KiB  
Review
Role of Nanomedicine-Based Therapeutics in the Treatment of CNS Disorders
by Zi-Hua Guo, Saadullah Khattak, Mohd Ahmar Rauf, Mohammad Azam Ansari, Mohammad N. Alomary, Sufyan Razak, Chang-Yong Yang, Dong-Dong Wu and Xin-Ying Ji
Molecules 2023, 28(3), 1283; https://doi.org/10.3390/molecules28031283 - 28 Jan 2023
Cited by 6 | Viewed by 3977
Abstract
Central nervous system disorders, especially neurodegenerative diseases, are a public health priority and demand a strong scientific response. Various therapy procedures have been used in the past, but their therapeutic value has been insufficient. The blood–brain barrier (BBB) and the blood–cerebrospinal fluid barrier [...] Read more.
Central nervous system disorders, especially neurodegenerative diseases, are a public health priority and demand a strong scientific response. Various therapy procedures have been used in the past, but their therapeutic value has been insufficient. The blood–brain barrier (BBB) and the blood–cerebrospinal fluid barrier is two of the barriers that protect the central nervous system (CNS), but are the main barriers to medicine delivery into the CNS for treating CNS disorders, such as brain tumors, Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease. Nanotechnology-based medicinal approaches deliver valuable cargos targeting molecular and cellular processes with greater safety, efficacy, and specificity than traditional approaches. CNS diseases include a wide range of brain ailments connected to short- and long-term disability. They affect millions of people worldwide and are anticipated to become more common in the coming years. Nanotechnology-based brain therapy could solve the BBB problem. This review analyzes nanomedicine’s role in medication delivery; immunotherapy, chemotherapy, and gene therapy are combined with nanomedicines to treat CNS disorders. We also evaluated nanotechnology-based approaches for CNS disease amelioration, with the intention of stimulating the immune system by delivering medications across the BBB. Full article
(This article belongs to the Special Issue Chemical Agents for Neurodegenerative Diseases)
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12 pages, 2023 KiB  
Review
Conformational Essentials Responsible for Neurotoxicity of Aβ42 Aggregates Revealed by Antibodies against Oligomeric Aβ42
by Chuli Song, Tianyu Zhang and Yingjiu Zhang
Molecules 2022, 27(19), 6751; https://doi.org/10.3390/molecules27196751 - 10 Oct 2022
Cited by 5 | Viewed by 1573
Abstract
Soluble aggregation of amyloid β-peptide 1-42 (Aβ42) and deposition of Aβ42 aggregates are the initial pathological hallmarks of Alzheimer’s disease (AD). The bipolar nature of Aβ42 molecule results in its ability to assemble into distinct oligomers and higher aggregates, which may drive some [...] Read more.
Soluble aggregation of amyloid β-peptide 1-42 (Aβ42) and deposition of Aβ42 aggregates are the initial pathological hallmarks of Alzheimer’s disease (AD). The bipolar nature of Aβ42 molecule results in its ability to assemble into distinct oligomers and higher aggregates, which may drive some of the phenotypic heterogeneity observed in AD. Agents targeting Aβ42 or its aggregates, such as anti-Aβ42 antibodies, can inhibit the aggregation of Aβ42 and toxicity of Aβ42 aggregates to neural cells to a certain extent. However, the epitope specificity of an antibody affects its binding affinity for different Aβ42 species. Different antibodies target different sites on Aβ42 and thus elicit different neuroprotective or cytoprotective effects. In the present review, we summarize significant information reflected by anti-Aβ42 antibodies in different immunotherapies and propose an overview of the structure (conformation)−toxicity relationship of Aβ42 aggregates. This review aimed to provide a reference for the directional design of antibodies against the most pathogenic conformation of Aβ42 aggregates. Full article
(This article belongs to the Special Issue Chemical Agents for Neurodegenerative Diseases)
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