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Cells
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Molecular Therapeutic Advances for Neurodegenerative Diseases
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Molecular Therapeutic Advances for Neurodegenerative Diseases

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 September 2025 | Viewed by 1496

Special Issue Editor

Dr. Vanessa Castelli

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Guest Editor
Department of Life, Health and Environmental Sciences, University of L’Aquila, 67100 L'Aquila, Italy
Interests: neurodegenerative diseases; neurodegeneration; neurological disorders; Parkinson’s disease; probiotics; neuropathic pain; stem cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The Special Issue, titled “Molecular Therapeutic Advances for Neurodegenerative Diseases”, focuses on the latest research and developments in understanding and treating neurodegenerative diseases at the molecular level. It aims to highlight innovative therapeutic strategies, including the identification of new molecular targets and the development of novel treatments to combat diseases, such as Alzheimer’s, Parkinson’s, stroke and other neurological disorders.

We are looking for a variety of manuscript types, including the following:

Original Research Articles: Detailed studies presenting new data on molecular mechanisms and therapeutic approaches for neurodegenerative diseases.

Review Articles: Comprehensive overviews of current knowledge and recent advancements in the field.

Communications: Brief reports on novel findings or preliminary data that can stimulate further research. 

Dr. Vanessa Castelli
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. Cells 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
  • neurodegeneration
  • neurological disorders

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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25 pages, 6761 KiB  
Article
Dopamine Receptor D3 Induces Transient, mTORC1-Dependent Autophagy That Becomes Persistent, AMPK-Mediated, and Neuroprotective in Experimental Models of Huntington’s Disease
by Diego Luis-Ravelo, Felipe Fumagallo-Reading, Alejandro Febles-Casquero, Jonathan Lopez-Fernandez, Daniel J. Marcellino and Tomas Gonzalez-Hernandez
Cells 2025, 14(9), 652; https://doi.org/10.3390/cells14090652 (registering DOI) - 29 Apr 2025
Abstract
Huntington disease’s (HD) is a neurodegenerative disorder caused by the expansion of a polyglutamine region (PolyQ) within the huntingtin protein (HTT). Mutated huntingtin (mHTT) is cytotoxic, particularly for striatal medium spiny neurons (MSNs), whose degeneration is the hallmark of HD. Autophagy inducers currently [...] Read more.
Huntington disease’s (HD) is a neurodegenerative disorder caused by the expansion of a polyglutamine region (PolyQ) within the huntingtin protein (HTT). Mutated huntingtin (mHTT) is cytotoxic, particularly for striatal medium spiny neurons (MSNs), whose degeneration is the hallmark of HD. Autophagy inducers currently available promote the clearance of toxic proteins. However, due to their low selectivity and the possibility that prolonged autophagy hampers essential processes in unaffected cells, researchers have questioned their benefits in neurodegenerative diseases. Since MSNs express dopamine receptors D2 (DRD2) and D3 (DRD3) and DRD2/DRD3 agonists may activate autophagy, here, we explored how healthy and mHTT-challenged cells respond to prolonged DRD2/DRD3 agonist treatment. Autophagy activation and its effects on mHTT/polyQ clearance were studied in R6/1 mice (a genetic model of HD), their wild-type littermates, and DRD2- and DRD3-HEK cells expressing a pathogenic (Q74) and a non-pathogenic (Q23) polyQ fragment of mHTT treated with the DRD2/DRD3 agonist pramipexole. Two forms of DRD3-mediated autophagy were found: a transient mTORC1-dependent in WT mice and Q23-DRD3-HEK cells and a persistent AMPK-ULK1-activated in R6/1 mice and Q74-DRD3-HEK cells. This also promoted a robust clearance of soluble mHTT/polyQ and neuroprotection in striatal neurons and DRD3-HEK cells. The findings indicate that DRD3-induced autophagy may be a safe, disease-modifying intervention in HD patients. Full article
(This article belongs to the Special Issue Molecular Therapeutic Advances for Neurodegenerative Diseases)
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Review

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19 pages, 889 KiB  
Review
Therapeutic Potential of Mesenchymal Stem Cell-Derived Extracellular Vesicles in the Treatment of Parkinson’s Disease
by Ana Volarevic, Carl Randall Harrell, Aleksandar Arsenijevic, Valentin Djonov and Vladislav Volarevic
Cells 2025, 14(8), 600; https://doi.org/10.3390/cells14080600 - 16 Apr 2025
Viewed by 379
Abstract
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the gradual loss of dopamine-producing neurons. Oxidative stress, mitochondrial dysfunction, detrimental immune response, and neuroinflammation are mainly responsible for the injury and degeneration of dopaminergic neurons in the brains of patients suffering from [...] Read more.
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the gradual loss of dopamine-producing neurons. Oxidative stress, mitochondrial dysfunction, detrimental immune response, and neuroinflammation are mainly responsible for the injury and degeneration of dopaminergic neurons in the brains of patients suffering from PD. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have emerged as a promising therapeutic approach for treating PD due to their ability to suppress the activation of inflammatory immune cells and enhance the viability and function of dopamine-producing neurons. MSC-EVs can easily bypass the blood-brain barrier and deliver their cargo (neuroprotective factors, immunosuppressive proteins, and microRNAs) to injured dopamine-producing neurons and brain-infiltrated inflammatory immune cells. A large number of recently published experimental studies demonstrated that MSC-EVs efficiently alleviated PD-related motor and behavioral deficits in animal models, indicating that MSC-EVs should be considered as potentially new therapeutic agents for the treatment of PD. Accordingly, in this review article, we summarized current knowledge about the therapeutic potential of MSCs-EVs in the treatment of PD, paving the way for their future clinical use in the treatment of neurodegenerative and neuroinflammatory disorders. Full article
(This article belongs to the Special Issue Molecular Therapeutic Advances for Neurodegenerative Diseases)
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18 pages, 2196 KiB  
Review
Neuronal Cell Rearrangement During Aging: Antioxidant Compounds as a Potential Therapeutic Approach
by Erjola Bej, Patrizia Cesare, Michele d’Angelo, Anna Rita Volpe and Vanessa Castelli
Cells 2024, 13(23), 1945; https://doi.org/10.3390/cells13231945 - 23 Nov 2024
Cited by 1 | Viewed by 984
Abstract
Aging is a natural process that leads to time-related changes and a decrease in cognitive abilities, executive functions, and attention. In neuronal aging, brain cells struggle to respond to oxidative stress. The structure, function, and survival of neurons can be mediated by different [...] Read more.
Aging is a natural process that leads to time-related changes and a decrease in cognitive abilities, executive functions, and attention. In neuronal aging, brain cells struggle to respond to oxidative stress. The structure, function, and survival of neurons can be mediated by different pathways that are sensitive to oxidative stress and age-related low-energy states. Mitochondrial impairment is one of the most noticeable signs of brain aging. Damaged mitochondria are thought to be one of the main causes that feed the inflammation related to aging. Also, protein turnover is involved in age-related impairments. The brain, due to its high oxygen usage, is particularly susceptible to oxidative damage. This review explores the mechanisms underlying neuronal cell rearrangement during aging, focusing on morphological changes that contribute to cognitive decline and increased susceptibility to neurodegenerative diseases. Potential therapeutic approaches are discussed, including the use of antioxidants (e.g., Vitamin C, Vitamin E, glutathione, carotenoids, quercetin, resveratrol, and curcumin) to mitigate oxidative damage, enhance mitochondrial function, and maintain protein homeostasis. This comprehensive overview aims to provide insights into the cellular and molecular processes of neuronal aging and highlight promising therapeutic avenues to counteract age-related neuronal deterioration. Full article
(This article belongs to the Special Issue Molecular Therapeutic Advances for Neurodegenerative Diseases)
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