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Cells
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Novel and Experimental Strategies for the Treatment of Neurodegenerative Diseases
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Novel and Experimental Strategies for the Treatment of Neurodegenerative Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Neuroscience".

Deadline for manuscript submissions: closed (10 April 2026) | Viewed by 9879

Special Issue Editors

Prof. Dr. Morten Meyer

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Guest Editor
Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark J.B. Winslows Vej 21, St., DK-5000 Odense, Denmark
Interests: Parkinson’s disease pathogenesis; neurodegeneration; stem cells; dopaminergic differentiation; neurotrophic factors; neuroprotection; cell replacement therpy; bioimaging; regenerative medicin
Special Issues, Collections and Topics in MDPI journals
Dr. Justyna Okarmus

E-Mail Website
Guest Editor
Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, J.B. Winslows Vej 21, DK-5000 Odense, Denmark
Interests: Parkinson’s disease pathogenesis; stem cells; dopaminergic differentiation; neurodegeneration; neuroprotection; neurotrophic factors; bioimaging; cell replacement therapy; regenerative medicine

Special Issue Information

Dear Colleagues,

In 2024, despite remarkable advancements in biomedical research, neurodegenerative disorders such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Huntington’s disease (HD), and Amyotrophic Lateral Sclerosis (ALS) remain challenging to treat effectively, and no cures exist. Conventional therapies have primarily focused on symptom management, but these approaches have not been able to stop or reverse disease progression. As our knowledge of the pathogenesis of these conditions increases, the need for novel and effective treatments becomes more urgent.

This Special Issue of Cells, titled "Novel and Experimental Strategies for the Treatment of Neurodegenerative Diseases", aims to present cutting-edge research and emerging therapeutic strategies that hold promise for modifying disease progression. We are particularly interested in highlighting advances in the following:

  • Stem Cell Transplantation: utilizing stem cells to replace damaged neurons, support neural growth, and modulate immune responses;
  • Immunotherapy: using the body's immune system to target and neutralize pathological proteins and reduce neuroinflammation;
  • Gene Therapy: employing technologies such as CRISPR/Cas9 and viral vectors to correct genetic mutations and provide long-term solutions for genetic neurodegenerative diseases;
  • Focused Ultrasound (FUS): using this non-invasive technique to enhance drug delivery to the brain by temporarily opening the blood–brain barrier for precise targeting;
  • Neuroprotective Agents: developing small molecule drugs that protect neurons from damage by targeting pathways involved in oxidative stress, mitochondrial dysfunction, and protein misfolding.

This Special Issue seeks contributions from both basic and clinical researchers in the form of original research articles and comprehensive reviews. We invite you to contribute your research and look forward to receiving insightful manuscripts, as we aim to stimulate further research that could lead to breakthroughs in the treatment of neurodegenerative diseases.

Prof. Dr. Morten Meyer
Dr. Justyna Okarmus
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 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-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
  • experimental treatments
  • stem cell transplantation
  • immunotherapy
  • gene therapy
  • focused ultrasound
  • neuroprotective agents
  • Parkinson's disease
  • Alzheimer's disease
  • Huntington’s disease
  • amyotrophic lateral sclerosis

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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

15 pages, 13819 KB  
Article
Preclinical Evaluation of the Assembly Modulator PAV-615 in a Mouse Model of C9orf72-Associated ALS/FTD
by Jingfen Su, Jorge Alaiz Noya, Anuradha F. Lingappa, Dennis Solas, Jimei Tong, Lillian Daughrity, Monica Castanedes-Casey, Aishe Kurti, Dennis W. Dickson, Vishwanath R. Lingappa, Leonard Petrucelli and Yongjie Zhang
Cells 2025, 14(24), 2012; https://doi.org/10.3390/cells14242012 - 17 Dec 2025
Viewed by 990
Abstract
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are fatal neurodegenerative diseases that share clinical and pathological features, as well as genetic causes. A G4C2 repeat expansion in chromosome 9 open reading frame 72 (C9orf72) is the most [...] Read more.
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are fatal neurodegenerative diseases that share clinical and pathological features, as well as genetic causes. A G4C2 repeat expansion in chromosome 9 open reading frame 72 (C9orf72) is the most common genetic cause of ALS and FTD, collectively referred to as c9ALS/FTD. Assembly modulation is a new therapeutic approach which appears to target allosteric sites on aberrant forms of multi-protein complexes and restore them to the healthy state. Recent findings demonstrate that tetrahydroisoquinolone (THIQ)-based protein assembly modulators can ameliorate ALS/FTD-associated phenotypes in cellular and animal models. In the present study, we investigated the effects of PAV-615, a novel and advanced THIQ-based modulator, in a c9ALS/FTD mouse model expressing 149 G4C2 repeat expansions (referred to as 149R mouse model). Specifically, PAV-615 was administered to 5-month-old 149R mice via intraperitoneal injection for one month. Motor function was evaluated using the hang wire test, while anxiety-like behavior and hyperactivity were assessed using the open-field test. Pathological markers, including dipeptide repeat (DPR) proteins, phosphorylated TAR DNA-binding protein 43 (pTDP-43) and ataxin 2-positive stress granules, were quantified by Meso Scale Discovery and immunohistochemistry assays. Compared with vehicle-treated controls, PAV-615 significantly improved motor performance and modestly reduced anxiety-like behavior and hyperactivity in 149R mice. Moreover, PAV-615 treatment significantly decreased cortical DPR, pTDP-43 and ataxin 2-positive stress granule burdens. These results support assembly modulation as a promising therapeutic approach treatment of ALS/FTD. Full article
(This article belongs to the Special Issue Novel and Experimental Strategies for the Treatment of Neurodegenerative Diseases)
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14 pages, 2097 KB  
Article
Angiotensin-(1-7) Provides Potent Long-Term Neurorepair/Neuroregeneration in a Rodent White Matter Stroke Model: Nonarteritic Ischemic Optic Neuropathy (rNAION)
by Kwang Min Woo, Yan Guo, Zara Mehrabian, Thomas Walther, Neil R. Miller and Steven L. Bernstein
Cells 2025, 14(4), 289; https://doi.org/10.3390/cells14040289 - 15 Feb 2025
Cited by 3 | Viewed by 2079
Abstract
Nonarteritic anterior ischemic optic neuropathy (NAION) is an ischemic lesion of the anterior optic nerve (ON), currently untreatable due to the length of time from symptom onset until treatment. We evaluated angiotensin-(1-7) (Ang-(1-7)): the MAS1-receptor ligand, as a possible NAION treatment using the [...] Read more.
Nonarteritic anterior ischemic optic neuropathy (NAION) is an ischemic lesion of the anterior optic nerve (ON), currently untreatable due to the length of time from symptom onset until treatment. We evaluated angiotensin-(1-7) (Ang-(1-7)): the MAS1-receptor ligand, as a possible NAION treatment using the rodent NAION model (rNAION). Long-Evans rats were unilaterally rNAION-induced. One-day post-induction, lesion severity was quantified via optic nerve head (ONH) edema using spectral domain optical coherence tomography. Animals meeting rNAION induction criteria were randomized into (1) Subcutaneous Ang-(1-7) infusion for 28 days and (2) Vehicle. Visual function was assessed using both visual acuity and flash visual evoked potentials (fVEP). Tissues were collected >30d and RGC neurons were quantified by stereology. ONs were histologically examined for inflammation. Ang-(1-7) improved post-rNAION visual function. Ang-(1-7)-treated animals showed improved visual acuity (ANCOVA: p = 0.0084) and improved fVEP amplitudes (ANCOVA: p = 0.0378) vs vehicle controls. The relative degree of improvement correlated with ONH edema severity. Treated animals showed trends towards increased RGC survival, and reduced optic nerve inflammatory cell infiltration. Ang-(1-7) is the first agent effective ≥1 day after rNAION induction. Ang-(1-7) type agonists may be useful in improving long-term function and neuronal survival in clinical NAION and other forms of white matter ischemia. Full article
(This article belongs to the Special Issue Novel and Experimental Strategies for the Treatment of Neurodegenerative Diseases)
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18 pages, 3612 KB  
Article
810-nm Photobiomodulation Evokes Glutamate Release in Normal and Rotenone-Dysfunctional Cortical Nerve Terminals by Modulating Mitochondrial Energy Metabolism
by Silvia Ravera, Elisa Farsetti, Guido Maura, Manuela Marcoli, Matteo Bozzo, Chiara Cervetto and Andrea Amaroli
Cells 2025, 14(2), 67; https://doi.org/10.3390/cells14020067 - 7 Jan 2025
Cited by 8 | Viewed by 5977
Abstract
The dysfunction of mitochondria, the primary source of cellular energy and producer of reactive oxygen species (ROS), is associated with brain aging and neurodegenerative diseases. Scientific evidence indicates that light in the visible and near-infrared spectrum can modulate mitochondrial activity, a phenomenon known [...] Read more.
The dysfunction of mitochondria, the primary source of cellular energy and producer of reactive oxygen species (ROS), is associated with brain aging and neurodegenerative diseases. Scientific evidence indicates that light in the visible and near-infrared spectrum can modulate mitochondrial activity, a phenomenon known in medicine as photobiomodulation therapy (PBM-t). The beneficial effects of PBM-t on dementia and neurodegeneration have been reviewed in the literature. However, the molecular mechanisms underlying these findings have yet to be fully elucidated. This study investigates the mechanism behind dose-dependent glutamate release in nerve terminals after irradiation with 810 nm, 1 W for 60 s continuous, 1 cm2, 1 W/cm2, 60 J, 60 J/cm2 (810 nm-1 W) or 810 nm, 0.1 W for 60 s continuous, 1 cm2, 0.1 W/cm2, 6 J, 6 J/cm2 (810 nm-0.1 W), focusing on mitochondrial activities. The results show that PBM modulated the mitochondrial metabolism of cortical nerve terminals and supported a power-dependent increase in oxidative phosphorylation (OxPhos) activity when stimulated with pyruvate plus malate (P/M) or succinate (succ) as respiratory substrates. The PBM-induced increase in OxPhos was sensitive to adding rotenone (Complex I inhibitor) and antimycin A (Complex III inhibitor) when synaptosomes were stimulated with P/M, but only to antimycin A when stimulated with succ. This allowed us to observe that the glutamate efflux, disrupted in the presence of rotenone, was partially restored by PBM due to the increase in the OxPhos pathway led by Complex II. This evidence suggests that PBM, acting on mitochondria, could facilitate physiological communication within the neuron-astrocyte network through vesicular glutamate release, potentially regulating healthy brain function and brain dysfunction. Full article
(This article belongs to the Special Issue Novel and Experimental Strategies for the Treatment of Neurodegenerative Diseases)
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