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Biomedicines
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Mechanisms and Novel Therapeutic Approaches for Neurodegenerative Diseases (3rd Edition)
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Mechanisms and Novel Therapeutic Approaches for Neurodegenerative Diseases (3rd Edition)

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

Deadline for manuscript submissions: 30 November 2026 | Viewed by 4995

Editor

Dr. Fernando Cardona

E-Mail Website
Guest Editor
Instituto de Biomedicina de Valencia-CSIC, 46010 Valencia, Spain
Interests: genetics; molecular biology; biochemistry; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are among the most prevalent health challenges of older age, profoundly affecting patient autonomy and imposing a significant burden on public health and healthcare systems.

Although certain molecular and cellular pathways are shared across multiple neurodegenerative conditions, others are disease-specific, and in many cases, the underlying mechanisms remain only partially understood. Even when the mechanisms are known, effective interventions to prevent, slow, or halt neurodegeneration remain limited.

This Special Issue invites original research articles and comprehensive reviews that explore the molecular and cellular mechanisms driving neurodegeneration and that advance potential therapeutic approaches. Manuscripts addressing related subjects are also welcome.

Dr. Fernando Cardona
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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

  • neurodegenerative diseases
  • cellular mechanisms
  • molecular mechanisms
  • mutations
  • neurodegeneration models
  • protein misfolding
  • protein aggregation
  • neuronal death
  • molecular therapy
  • cellular therapy
  • therapeutics
  • medical chemistry
  • drug screening

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Related Special Issues

Published Papers (3 papers)

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Research

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14 pages, 2004 KB  
Article
Isotopic H/D Exchange in Hydrogen Bonds Between the Nitrogenous Bases of the CAG Repeat Tract Makes It Possible to Stabilize Its Expansion in the ATXN2 Gene
by Anna Dorohova, Luis Velázquez-Pérez, Mikhail Drobotenko, Oksana Lyasota, Jose Luis Hernandez-Caceres, Roberto Rodriguez-Labrada, Alexandr Svidlov, Olga Leontyeva, Yury Nechipurenko and Stepan Dzhimak
Biomedicines 2025, 13(11), 2708; https://doi.org/10.3390/biomedicines13112708 - 4 Nov 2025
Viewed by 949
Abstract
Background: The isotopic composition of the body’s internal environment can affect its functional state. Such effects are realized, among other things, by inserting deuterium atoms into hydrogen bonds between pairs of nitrogenous bases of DNA molecules and modifying their mechanical properties. Methods [...] Read more.
Background: The isotopic composition of the body’s internal environment can affect its functional state. Such effects are realized, among other things, by inserting deuterium atoms into hydrogen bonds between pairs of nitrogenous bases of DNA molecules and modifying their mechanical properties. Methods: This study uses a coarse-grained mathematical model of DNA. Results: It has been established that in a certain range of the magnitude of the torque, with the presence of a deuterium atom within it, stabilization of the CAG repeat tract is observed. In addition, it was found that, regardless of which base pair the deuterium atom falls into in the CAG repeat tract, its stability increases and the probability of hairpin formation decreases, which may interfere with the reading of genetic information from the site encoding glutamine. Conclusions: Single H/D substitutions in the CAG repeat tract of the ATXN2 gene increase its stability by reducing the formation of open states, regardless of the position of deuterium. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Neurodegenerative Diseases (3rd Edition))
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Review

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17 pages, 1369 KB  
Review
Coenzyme A in Brain Biology and Neurodegeneration
by Dejun Zhang, Charlie Brett, Jason Cho, Tammaryn Lashley and Ivan Gout
Biomedicines 2026, 14(1), 69; https://doi.org/10.3390/biomedicines14010069 - 29 Dec 2025
Cited by 2 | Viewed by 1622
Abstract
Coenzyme A (CoA) biology has been extensively studied in health and disease due to the central role of CoA in numerous metabolic and signalling processes. CoA is essential for all living organisms, and its biosynthesis and homeostasis are tightly regulated by nutrient availability, [...] Read more.
Coenzyme A (CoA) biology has been extensively studied in health and disease due to the central role of CoA in numerous metabolic and signalling processes. CoA is essential for all living organisms, and its biosynthesis and homeostasis are tightly regulated by nutrient availability, mitogenic stimuli, and stress signals. Disruptions in CoA biosynthesis, caused by inborn mutations in genes encoding enzymes of the CoA biosynthetic pathway (such as PANK2 and CoASy), lead to neurodegeneration, indicating the critical role of CoA/CoA thioesters in the function and viability of neuronal cells. The molecular mechanisms linking CoA deficiency to neurodegeneration remain unknown, but recent studies have highlighted the involvement of disrupted metabolism and redox homeostasis. The antioxidant function of CoA, mediated by protein CoAlation, has recently emerged as a novel and important mechanism of redox regulation. This review highlights well-established principles of CoA in neuronal metabolism and summarises recent advances in our understanding of its role in adaptive responses to oxidative and metabolic stress. The identification of enzymes involved in the CoAlation/deCoAlation cycle, together with the development of novel analytical tools and methodologies, may provide new insights into the discovery of more effective diagnostic and therapeutic approaches for targeting neurodegenerative diseases. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Neurodegenerative Diseases (3rd Edition))
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Other

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25 pages, 1103 KB  
Systematic Review
Mesenchymal Stem Cell-Based Therapies Applied in Neurological Diseases: A Systematic Review
by Ana Trabulo, Patrícia Sousa, Rui Alvites and Ana Colette Maurício
Biomedicines 2026, 14(2), 475; https://doi.org/10.3390/biomedicines14020475 - 21 Feb 2026
Cited by 2 | Viewed by 1997
Abstract
Background/Objectives: Neurodegenerative diseases (NDs) have a severe impact on patients’ quality of life, and effective treatments remain limited. As the focus is on treating the symptoms, the root cause of the problem is commonly not addressed. Mesenchymal stem cells show an emerging [...] Read more.
Background/Objectives: Neurodegenerative diseases (NDs) have a severe impact on patients’ quality of life, and effective treatments remain limited. As the focus is on treating the symptoms, the root cause of the problem is commonly not addressed. Mesenchymal stem cells show an emerging potential due to the ability for self-renewal combined with their capability for differentiation into various cell lines, which makes them a strong candidate for regenerative therapies in general, and for application in neurological issues in particular. This article provides an overview of the safety, efficacy, and challenges associated with the use of mesenchymal stem cells (MSCs) and their derived secretome in clinical and preclinical models of Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD) and amyotrophic lateral sclerosis (ALS). Methods: A systematic search was conducted on PubMed to identify published studies providing clinical and preclinical evidence on the use of MSCs in neurodegenerative disorders. Results: Overall, the literature consistently indicates that MSCs and their derivatives exert disease-modifying effects across multiple NDs. Across AD, PD, HD and ALS, preclinical studies uniformly report improvements in behavioural outcomes, attenuation of neuroinflammation, and neuroprotective effects, largely mediated by MSCs’ paracrine signalling rather than direct cell replacement. Clinical studies to date consistently support the safety and feasibility of MSC-based therapies, while efficacy signals remain modest, heterogeneous and predominantly short-term, highlighting the need for larger, well-controlled trials. Conclusions: Integration of genetic engineering, preconditioning, and EV technology may represent an emerging therapeutic approach that may complement existing neuroregeneration treatments, offering a scalable and minimally invasive frontier to improve long-term clinical outcomes in patients with AD, PD, HD, and ALS. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Neurodegenerative Diseases (3rd Edition))
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