Submit to Biomedicines Review for Biomedicines Propose a Special Issue

Journal Browser

Amyloid β, Tau, and α-Synuclein Aggregates in the Pathogenesis, Prognosis, and Therapeutics for Neurodegenerative Diseases

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 8101

Share This Special Issue

Special Issue Editor

Dr. Ashok Iyaswamy

E-Mail Website
Guest Editor

School of Chinese Medicine, Hong Kong Baptist University, Hong Kong
Interests: Alzheimer’s disease; blood–brain barrier permeable drugs; biomaterials; autophagy inducers; animal models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) is characterized by the progressive and irreversible decline of memory, thinking and cognitive abilities, and is the most common form of neurodegenerative dementia. More than 55 million people suffer from dementia worldwide, and the patient number is anticipated to rise to 139 million by 2050 because of population ageing. Presently, AD remains incurable, and the high failure rate of clinical trials for AD-related drugs have raised the need to understand the symptoms of AD. Worst of all, its underlying etiology is still not well understood. Therefore, AD has posed tremendous challenges for both scientific researchers and medical experts to tackle the unresolved issues in early detection, diagnostics and therapeutics for AD. The use of advanced technology for the treatment of AD in diagnostics, brain delivery, and therapeutics will help to yield solutions from bench to bedside in AD therapy.

This Research Topic welcomes contributions, in the form of original research articles or reviews and opinions, to address/summarize the challenges and understanding of Amyloid β, Tau, and α-Synuclein Aggregates in the Pathogenesis, Prognosis, and Therapeutics for Neurodegenerative Diseases.

Dr. Ashok Iyaswamy
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. Biomedicines 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 2600 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

Alzheimer’s disease
Parkinson’s disease
autophagy-lysosomal pathway
small molecule
phytochemicals
therapeutics
tau pathology
α-synuclein

Published Papers (4 papers)

Download All Papers

Research

Jump to: Review

11 pages, 258 KiB

Open AccessArticle

Alzheimer Disease Associated Loci: APOE Single Nucleotide Polymorphisms in Marmara Region

by Aya Badeea Ismail, Mehmet Sait Dundar, Cemre Ornek Erguzeloglu, Mahmut Cerkez Ergoren, Adem Alemdar, Sebnem Ozemri Sag and Sehime Gulsun Temel

Biomedicines 2024, 12(5), 968; https://doi.org/10.3390/biomedicines12050968 - 27 Apr 2024

Viewed by 525

Abstract

Alzheimer’s disease (AD) is a major global health challenge, especially among individuals aged 65 or older. According to population health studies, Turkey has the highest AD prevalence in the Middle East and Europe. To accurately determine the frequencies of common and rare APOE single nucleotide polymorphisms (SNPs) in the Turkish population residing in the Marmara Region, we conducted a retrospective study analyzing APOE variants in 588 individuals referred to the Bursa Uludag University Genetic Diseases Evaluation Center. Molecular genotyping, clinical exome sequencing, bioinformatics analysis, and statistical evaluation were employed to identify APOE polymorphisms and assess their distribution. The study revealed the frequencies of APOE alleles as follows: ε4 at 9.94%, ε2 at 9.18%, and ε3 at 80.68%. The gender-based analysis in our study uncovered a tendency for females to exhibit a higher prevalence of mutant genotypes across various SNPs. The most prevalent haplotype observed was ε3/ε3, while rare APOE SNPs were also identified. These findings align with global observations, underscoring the significance of genetic diversity and gender-specific characteristics in comprehending health disparities and formulating preventive strategies. Full article

(This article belongs to the Special Issue Amyloid β, Tau, and α-Synuclein Aggregates in the Pathogenesis, Prognosis, and Therapeutics for Neurodegenerative Diseases)

10 pages, 1519 KiB

Open AccessArticle

Astemizole, a Second-Generation Histamine H1-Receptor Antagonist, Did Not Attenuate the Aggregation Process of α-Synuclein In Vitro

by Jung Il Choi, Hyunjo Lee, Dong Jun Kim, Eun Suk Park, Kyung Yeon Lee and Hui-Jun Yang

Biomedicines 2024, 12(3), 611; https://doi.org/10.3390/biomedicines12030611 - 8 Mar 2024

Viewed by 803

Abstract

The antihistamine astemizole has shown disease-modifying effects in several preclinical disease models of Parkinson’s disease (PD). Astemizole also interacts with an anomalous aggregation of Alzheimer’s disease-related amyloid-β (Aβ) peptide and has inhibitory activity on the human prion protein PrP^Sc. We hypothesized that the proposed preclinical benefits of astemizole on PD can be associated with the attenuation of pathological α-synuclein (α-syn) aggregation. We tested the effects of astemizole on the fibrillation processes of amyloid peptides using thioflavin T aggregation monitoring, Congo red spectral analysis, cell viability study, and transmission electron microscopic imaging. We found that astemizole did not inhibit α-syn aggregation in vitro even at a high molar ratio but inhibited the assembly of Aβ aggregates. Our results suggest that the inhibitory effect of astemizole on amyloid formation is target-protein selective, and the proposed beneficial effects of this compound observed in translational PD models might not be due to its ameliorating effects on α-syn aggregation. Full article

(This article belongs to the Special Issue Amyloid β, Tau, and α-Synuclein Aggregates in the Pathogenesis, Prognosis, and Therapeutics for Neurodegenerative Diseases)

► Show Figures

Figure 1

13 pages, 4283 KiB

Open AccessArticle

Gene Set Enrichment Analysis and Genetic Experiment Reveal Changes in Cell Signaling Pathways Induced by α-Synuclein Overexpression

by Yusong Huang, Dongjing Wen, Yao Yuan and Wenfeng Chen

Biomedicines 2023, 11(2), 263; https://doi.org/10.3390/biomedicines11020263 - 18 Jan 2023

Viewed by 3816

Abstract

Abnormal accumulation of alpha synuclein (α-Syn) in sporadic and familial Parkinson’s disease (PD) may be a key step in its pathogenesis. In this study, the expression matrix of the GSE95427 dataset after α-Syn overexpression in human glioma cell line H4 was obtained from the GEO database. We used the Gene Set Enrichment Analysis (GSEA) method to reanalyze this dataset to evaluate the possible functions of α-Syn. The results showed that the tumor necrosis factor alpha (TNF-α) signal was significantly activated in α-Syn-overexpressing cells, and oxidative phosphorylation signal, extracellular matrix signal, cell cycle related signal and fatty acid metabolism signal were significantly inhibited. Moreover, we employed the α-Syn-expressing transgenic Drosophila model of Parkinson’s disease and knocked-down eiger, a TNF superfamily ligand homologue, indicating that the TNF-α pathway plays a role in the common pathogenesis of synucleinopathies. Our analysis based on GSEA data provides more clues for a better understanding of α-Syn function. Full article

(This article belongs to the Special Issue Amyloid β, Tau, and α-Synuclein Aggregates in the Pathogenesis, Prognosis, and Therapeutics for Neurodegenerative Diseases)

► Show Figures

Figure 1

Review

Jump to: Research

13 pages, 4045 KiB

Open AccessReview

Impact and Advances in the Role of Bacterial Extracellular Vesicles in Neurodegenerative Disease and Its Therapeutics

by Ashok Iyaswamy, Kejia Lu, Xin-Jie Guan, Yuxuan Kan, Chengfu Su, Jia Liu, Ravindran Jaganathan, Karthick Vasudevan, Jeyakumari Paul, Abhimanyu Thakur and Min Li

Biomedicines 2023, 11(7), 2056; https://doi.org/10.3390/biomedicines11072056 - 21 Jul 2023

Cited by 8 | Viewed by 2507

Abstract

Bacterial Extracellular Vesicles (BEVs) possess the capability of intracellular interactions with other cells, and, hence, can be utilized as an efficient cargo for worldwide delivery of therapeutic substances such as monoclonal antibodies, proteins, plasmids, siRNA, and small molecules for the treatment of neurodegenerative diseases (NDs). BEVs additionally possess a remarkable capacity for delivering these therapeutics across the blood–brain barrier to treat Alzheimer’s disease (AD). This review summarizes the role and advancement of BEVs for NDs, AD, and their treatment. Additionally, it investigates the critical BEV networks in the microbiome–gut–brain axis, their defensive and offensive roles in NDs, and their interaction with NDs. Furthermore, the part of BEVs in the neuroimmune system and their interference with ND, as well as the risk factors made by BEVs in the autophagy–lysosomal pathway and their potential outcomes on ND, are all discussed. To conclude, this review aims to gain a better understanding of the credentials of BEVs in NDs and possibly discover new therapeutic strategies. Full article

(This article belongs to the Special Issue Amyloid β, Tau, and α-Synuclein Aggregates in the Pathogenesis, Prognosis, and Therapeutics for Neurodegenerative Diseases)

► Show Figures