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Biology
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Development of Therapeutics for the Treatment of Alzheimer’s Disease
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Development of Therapeutics for the Treatment of Alzheimer’s Disease

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 13022

Special Issue Editor

Dr. Stephen P. Wren

E-Mail Website
Guest Editor
Department of Chemical and Pharmaceutical Sciences, Kingston University London, London KT1 2EE, UK
Interests: organic and medicinal chemistry; drug discovery and development; signaling molecules; chemical and biosensors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer’s disease affects 30–35 million people across the globe and is likely to present an increasing demand on medical, social care and economic resources. This disease is not just a function of growing old; there are certain molecular mechanisms/hypotheses that drive the development of pathological damage and cognitive decline. These include tau phosphorylation, neuroinflammation, the role of N-methyl-D-aspartate receptors and several others.

This Special Issue focuses on recent research advances around the development of therapeutics for the treatment of Alzheimer’s disease. Original articles related to novel biological approaches in this area or the discovery of small molecule/biologics for this type of dementia are warmly welcomed. Relevant reviews and papers detailing biological pathways will be considered for acceptance. In addition, articles that impinge on pharmacological studies, innovative in vitro/in vivo work, in silico methods and/or chemically driven studies are also invited.

Dr. Stephen Wren
Guest Editor

Manuscript Submission Information

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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. Biology 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 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

  • cognitive decline
  • Alzheimer’s disease
  • tau phosphorylation
  • therapeutics
  • neuroinflammation

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Published Papers (3 papers)

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Research

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31 pages, 12793 KiB  
Article
Mesenchymal Stem Cells and Begacestat Mitigate Amyloid-β 25–35-Induced Cognitive Decline in Rat Dams and Hippocampal Deteriorations in Offspring
by Asmaa Gaber, Osama M. Ahmed, Yasser A. Khadrawy, Khairy M. A. Zoheir, Rasha E. Abo-ELeneen, Mohamed A. Alblihed and Ahlam M. Elbakry
Biology 2023, 12(7), 905; https://doi.org/10.3390/biology12070905 - 25 Jun 2023
Cited by 2 | Viewed by 1707
Abstract
Alzheimer’s disease (AD) is the most common cause of age-related neurodegeneration and cognitive decline. AD more commonly occurs in females than in males, so it is necessary to consider new treatments specifically targeting this population. The present study investigated the protective effects of [...] Read more.
Alzheimer’s disease (AD) is the most common cause of age-related neurodegeneration and cognitive decline. AD more commonly occurs in females than in males, so it is necessary to consider new treatments specifically targeting this population. The present study investigated the protective effects of Begacestat (γ-secretase inhibitor-953, GSI-953) and bone marrow-derived mesenchymal stem cells (BM-MSCs) during pregnancy on cognitive impairment in rat dams and neurodegeneration in offspring caused by the intracerebroventricular injection of Aβ 25–35 before pregnancy. The performances of dams injected with amyloid-β 25–35 (Aβ 25–35) during behavioral tests were significantly impaired. The offspring of Aβ 25–35-injected dams treated with BM-MSCs or GSI-953 showed a dramatically reduced number and size of activated microglial cells, enhancement in the processes length, and a decrease in the proinflammatory cytokine levels. Additionally, BM-MSC or GSI-953 therapy reduced Aβ 25–35-induced increases in tau phosphorylation and amyloid precursor protein levels in the neonates’ hippocampus and elevated the lower levels of glycogen synthase kinase-3 and brain-derived neurotrophic factor; moreover, reversed Aβ 25–35-induced alterations in gene expression in the neonatal hippocampus. Finally, the treatments with BM-MSC or GSI-953 are globally beneficial against Aβ 25–35-induced brain alterations, particularly by suppressing neural inflammation, inhibiting microglial cell activation, restoring developmental plasticity, and increasing neurotrophic signaling. Full article
(This article belongs to the Special Issue Development of Therapeutics for the Treatment of Alzheimer’s Disease)
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17 pages, 3273 KiB  
Article
The Oxindole Derivatives, New Promising GSK-3β Inhibitors as One of the Potential Treatments for Alzheimer’s Disease—A Molecular Dynamics Approach
by Przemysław Czeleń and Beata Szefler
Biology 2021, 10(4), 332; https://doi.org/10.3390/biology10040332 - 15 Apr 2021
Cited by 8 | Viewed by 2523
Abstract
The glycogen synthase kinase 3β (GSK-3β) is a protein kinase involved in regulating numerous physiological processes such as embryonic development, transcription, insulin action, cell division cycle and multiple neuronal functions. The overexpression of this enzyme is related to many diseases such as schizophrenia, [...] Read more.
The glycogen synthase kinase 3β (GSK-3β) is a protein kinase involved in regulating numerous physiological processes such as embryonic development, transcription, insulin action, cell division cycle and multiple neuronal functions. The overexpression of this enzyme is related to many diseases such as schizophrenia, Alzheimer’s disease, diabetes and cancer. One of the basic methods of treatment in these cases is the usage of ATP-competitive inhibitors. A significant group of such compounds are indirubin and its analogs, e.g., oxindole derivatives. The compounds considered in this work are 112 newly designed oxindole derivatives. In the first stage, such molecular properties of considered compounds as toxicity and LogP were estimated. The preliminary analysis of the binding capabilities of considered compounds towards the GSK-3β active site was conducted with the use of the docking procedure. Based on obtained molecular properties and docking simulations, a selected group of complexes that were analyzed in the molecular dynamics stage was nominated. The proposed procedure allowed for the identification of compounds such as Oxind_4_9 and Oxind_13_10, which create stable complexes with GSK-3β enzyme and are characterized by the highest values of binding affinity. The key interactions responsible for stabilization of considered ligand–protein complexes were identified, and their dynamic stability was also determined. Comparative analysis including analyzed compounds and reference molecule 3a, which is also an oxindole derivative with a confirmed inhibitory potential towards GSK3B protein, clearly indicates that the proposed compounds exhibit an analogous binding mechanism, and the obtained binding enthalpy values indicate a slightly higher binding potential than the reference molecule. Full article
(This article belongs to the Special Issue Development of Therapeutics for the Treatment of Alzheimer’s Disease)
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Review

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23 pages, 1462 KiB  
Review
DNA Methylation: A Promising Approach in Management of Alzheimer’s Disease and Other Neurodegenerative Disorders
by Gagandeep Kaur, Suraj Singh S. Rathod, Mohammed M. Ghoneim, Sultan Alshehri, Javed Ahmad, Awanish Mishra and Nabil A. Alhakamy
Biology 2022, 11(1), 90; https://doi.org/10.3390/biology11010090 - 7 Jan 2022
Cited by 41 | Viewed by 7648
Abstract
DNA methylation, in the mammalian genome, is an epigenetic modification that involves the transfer of a methyl group on the C5 position of cytosine to derive 5-methylcytosine. The role of DNA methylation in the development of the nervous system and the progression of [...] Read more.
DNA methylation, in the mammalian genome, is an epigenetic modification that involves the transfer of a methyl group on the C5 position of cytosine to derive 5-methylcytosine. The role of DNA methylation in the development of the nervous system and the progression of neurodegenerative diseases such as Alzheimer’s disease has been an interesting research area. Furthermore, mutations altering DNA methylation affect neurodevelopmental functions and may cause the progression of several neurodegenerative diseases. Epigenetic modifications in neurodegenerative diseases are widely studied in different populations to uncover the plausible mechanisms contributing to the development and progression of the disease and detect novel biomarkers for early prognosis and future pharmacotherapeutic targets. In this manuscript, we summarize the association of DNA methylation with the pathogenesis of the most common neurodegenerative diseases, such as, Alzheimer’s disease, Parkinson’s disease, Huntington diseases, and amyotrophic lateral sclerosis, and discuss the potential of DNA methylation as a potential biomarker and therapeutic tool for neurogenerative diseases. Full article
(This article belongs to the Special Issue Development of Therapeutics for the Treatment of Alzheimer’s Disease)
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