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Editorial Board Members’ Collection Series: Physiology and Drug Discovery of Neurodegenerative Diseases

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

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 8332

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Special Issue Editors

Prof. Dr. Hengming Ke

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Guest Editor

1. Department of Biochemistry and Biophysics, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
2. Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
Interests: X-ray protein crystallography; enzymology; structure-based drug design

Prof. Dr. Carlo M. Bergamini

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Guest Editor

Department of Biomedical Sciences and Specialist Surgery, Section of Biochemistry, Molecular Biology and Medical Genetics, University of Ferrara, Via Luigi Borsari 46, 44121 Ferrara, Italy
Interests: enzymology; protein chemistry; transglutaminase; gene regulation; oxidative damage

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute your work to a Special Issue of Biology entitled “Editorial Board Members’ Collection Series: Physiology and Drug Discovery of Neurodegenerative Diseases”. Neurodegenerative diseases are caused by the progressive loss of neuron structure in the process of neurodegeneration, which ultimately leads to neuron cell death. The major neurodegenerative diseases include Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, multiple sclerosis, Huntington’s disease, multiple-system atrophy, prion diseases, and Friedreich’s ataxia. Since there are currently no methods or treatments that can effectively reverse the progressive degeneration of neurons, these diseases are considered incurable.

The aim of this Special Issue is to collect articles that represent the current knowledge and progress in neurodegenerative diseases for dissemination to the readers, and to promote the progress of the field. In this Special Issue, original research articles and reviews are welcome. Although Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis are the major focuses of this Special Issue, any articles on neurodegenerative diseases are welcome.

We look forward to receiving your contributions.

Prof. Dr. Hengming Ke
Prof. Dr. Carlo M. Bergamini
Guest Editors

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. 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

neurodegenerative diseases
Alzheimer’s
Parkinson’s
Huntington’s
amyotrophic lateral sclerosis
multiple-system atrophy
prion diseases
Friedreich’s ataxia

Published Papers (3 papers)

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Research

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20 pages, 3242 KiB

Open AccessArticle

Adenosine Improves Mitochondrial Function and Biogenesis in Friedreich's Ataxia Fibroblasts Following L-Buthionine Sulfoximine-Induced Oxidative Stress

by Sze Yuen Lew, Nur Shahirah Mohd Hisam, Michael Weng Lok Phang, Syarifah Nur Syed Abdul Rahman, Rozaida Yuen Ying Poh, Siew Huah Lim, Mohd Amir Kamaruzzaman, Sze Chun Chau, Ka Chun Tsui, Lee Wei Lim and Kah Hui Wong

Biology 2023, 12(4), 559; https://doi.org/10.3390/biology12040559 - 06 Apr 2023

Cited by 1 | Viewed by 3215

Abstract

Adenosine is a nucleoside that is widely distributed in the central nervous system and acts as a central excitatory and inhibitory neurotransmitter in the brain. The protective role of adenosine in different pathological conditions and neurodegenerative diseases is mainly mediated by adenosine receptors. However, its potential role in mitigating the deleterious effects of oxidative stress in Friedreich’s ataxia (FRDA) remains poorly understood. We aimed to investigate the protective effects of adenosine against mitochondrial dysfunction and impaired mitochondrial biogenesis in L-buthionine sulfoximine (BSO)-induced oxidative stress in dermal fibroblasts derived from an FRDA patient. The FRDA fibroblasts were pre-treated with adenosine for 2 h, followed by 12.50 mM BSO to induce oxidative stress. Cells in medium without any treatments or pre-treated with 5 µM idebenone served as the negative and positive controls, respectively. Cell viability, mitochondrial membrane potential (MMP), aconitase activity, adenosine triphosphate (ATP) level, mitochondrial biogenesis, and associated gene expressions were assessed. We observed disruption of mitochondrial function and biogenesis and alteration in gene expression patterns in BSO-treated FRDA fibroblasts. Pre-treatment with adenosine ranging from 0–600 µM restored MMP, promoted ATP production and mitochondrial biogenesis, and modulated the expression of key metabolic genes, namely nuclear respiratory factor 1 (NRF1), transcription factor A, mitochondrial (TFAM), and NFE2-like bZIP transcription factor 2 (NFE2L2). Our study demonstrated that adenosine targeted mitochondrial defects in FRDA, contributing to improved mitochondrial function and biogenesis, leading to cellular iron homeostasis. Therefore, we suggest a possible therapeutic role for adenosine in FRDA. Full article

(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Physiology and Drug Discovery of Neurodegenerative Diseases)

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Review

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18 pages, 765 KiB

Open AccessReview

Neuroprotective Action of Humanin and Humanin Analogues: Research Findings and Perspectives

by Chrysoula-Evangelia Karachaliou and Evangelia Livaniou

Biology 2023, 12(12), 1534; https://doi.org/10.3390/biology12121534 - 16 Dec 2023

Viewed by 1275

Abstract

Humanin is a 24-mer peptide first reported in the early 2000s as a new neuroprotective/cytoprotective factor rescuing neuronal cells from death induced by various Alzheimer’s disease-associated insults. Nowadays it is known that humanin belongs to the novel class of the so-called mitochondrial-derived peptides (which are encoded by mitochondrial DNA) and has been shown to exert beneficial cytoprotective effects in a series of in vitro and/or in vivo experimental models of human diseases, including not only neurodegenerative disorders but other human diseases as well (e.g., age-related macular degeneration, cardiovascular diseases, or diabetes mellitus). This review article is focused on the presentation of recent in vitro and in vivo research results associated with the neuroprotective action of humanin as well as of various, mainly synthetic, analogues of the peptide; moreover, the main mode(s)/mechanism(s) through which humanin and humanin analogues may exert in vitro and in vivo regarding neuroprotection have been reported. The prospects of humanin and humanin analogues to be further investigated in the frame of future research endeavors against neurodegenerative/neural diseases have also been briefly discussed. Full article

(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Physiology and Drug Discovery of Neurodegenerative Diseases)

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32 pages, 2200 KiB

Open AccessReview

Polyherbal and Multimodal Treatments: Kaempferol- and Quercetin-Rich Herbs Alleviate Symptoms of Alzheimer’s Disease

by Claire Alexander, Ali Parsaee and Maryam Vasefi

Biology 2023, 12(11), 1453; https://doi.org/10.3390/biology12111453 - 20 Nov 2023

Cited by 1 | Viewed by 3308

Abstract

Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder impairing cognition and memory in the elderly. This disorder has a complex etiology, including senile plaque and neurofibrillary tangle formation, neuroinflammation, oxidative stress, and damaged neuroplasticity. Current treatment options are limited, so alternative treatments such as herbal medicine could suppress symptoms while slowing cognitive decline. We followed PRISMA guidelines to identify potential herbal treatments, their associated medicinal phytochemicals, and the potential mechanisms of these treatments. Common herbs, including Ginkgo biloba, Camellia sinensis, Glycyrrhiza uralensis, Cyperus rotundus, and Buplerum falcatum, produced promising pre-clinical results. These herbs are rich in kaempferol and quercetin, flavonoids with a polyphenolic structure that facilitate multiple mechanisms of action. These mechanisms include the inhibition of Aβ plaque formation, a reduction in tau hyperphosphorylation, the suppression of oxidative stress, and the modulation of BDNF and PI3K/AKT pathways. Using pre-clinical findings from quercetin research and the comparatively limited data on kaempferol, we proposed that kaempferol ameliorates the neuroinflammatory state, maintains proper cellular function, and restores pro-neuroplastic signaling. In this review, we discuss the anti-AD mechanisms of quercetin and kaempferol and their limitations, and we suggest a potential alternative treatment for AD. Our findings lead us to conclude that a polyherbal kaempferol- and quercetin-rich cocktail could treat AD-related brain damage. Full article

(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Physiology and Drug Discovery of Neurodegenerative Diseases)

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