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Cells
Special Issues
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 "Cells of the Nervous System".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 2363

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 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
  • 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 (2 papers)

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14 pages, 2097 KiB  
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
Viewed by 638
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 KiB  
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 1 | Viewed by 1397
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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