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Pharmaceuticals
Special Issues
Innovations in Therapeutic Strategies for Retinal and Neurodegenerative Diseases
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Innovations in Therapeutic Strategies for Retinal and Neurodegenerative Diseases

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 25 May 2026 | Viewed by 5229

Special Issue Editors

Dr. Tonking Bastola

E-Mail Website
Guest Editor
Hamilton Glaucoma Center and Viterbi Family Department of Ophthalmology and Shiley Eye Institute, University of California San Diego, La Jolla, CA 92093, USA
Interests: glaucoma; Alzheimer’s disease; neurodegeneration; neuroinflammation; neuroprotection; oxidative stress; mitochondrial dysfunction
Dr. Won-Kyu Ju

E-Mail Website
Guest Editor
Hamilton Glaucoma Center and Viterbi Family Department of Ophthalmology and Shiley Eye Institute, University of California San Diego, La Jolla, CA 92093, USA
Interests: glaucoma; Alzheimer’s disease; neurodegeneration; neuroinflammation; neuroprotection; oxidative stress; mitochondrial dysfunction

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases, including glaucoma, Alzheimer’s disease, and retinal disorders such as age-related macular degeneration and diabetic retinopathy, represent a significant global health burden due to their progressive nature and lack of curative treatments. These conditions share common pathological mechanisms, including neuroinflammation, oxidative stress, and neuronal dysfunction, highlighting opportunities for innovative therapeutic approaches.

This Special Issue aims to provide a platform for groundbreaking research and translational advances in the treatment of retinal and neurodegenerative diseases. It seeks to highlight novel therapeutic strategies, ranging from gene and cell therapies to advanced drug delivery systems, as well as diagnostic approaches designed to detect early disease biomarkers and personalize treatments.

Potential topics include, but are not limited to, the following:

  • Cellular and molecular mechanisms underlying retinal and neurodegenerative diseases;
  • Novel therapeutic interventions, including gene therapy, neuroprotection, and regenerative medicine;
  • Innovations in drug delivery platforms and biomaterials;
  • Advances in retinal prostheses and bioengineered tissues for vision restoration;
  • Neuroinflammation and oxidative stress as therapeutic targets;
  • Artificial intelligence and imaging technologies for early diagnosis and disease management;
  • Translational and clinical studies on emerging therapies.

This Special Issue welcomes contributions from diverse disciplines, including neuroscience, ophthalmology, molecular biology, pharmacology, and biomedical engineering. By bridging these fields, this issue aims to advance our understanding and treatment of complex retinal and neurodegenerative diseases.

Dr. Tonking Bastola
Dr. Won-Kyu Ju
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. Pharmaceuticals 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 2900 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

  • glaucoma
  • Alzheimer's diseases
  • retinal disease
  • neuroprotection
  • neuroinflammation

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

Published Papers (2 papers)

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Research

15 pages, 3730 KB  
Article
Efficacy of Tumor Necrosis Factor-α Inhibitor Adalimumab in Chronic Recurrent Vogt–Koyanagi–Harada Disease
by Junghoo Lee, Yoo-Ri Chung, Hae Rang Kim and Ji Hun Song
Pharmaceuticals 2025, 18(12), 1848; https://doi.org/10.3390/ph18121848 - 3 Dec 2025
Cited by 1 | Viewed by 1047
Abstract
Background/Objectives: Vogt–Koyanagi–Harada (VKH) disease is a bilateral granulomatous panuveitis that can progress to a chronic, relapsing phase. Patients refractory or intolerant to systemic corticosteroids and conventional immunomodulatory therapy pose a major therapeutic challenge, as persistent inflammation can lead to cumulative ocular damage and [...] Read more.
Background/Objectives: Vogt–Koyanagi–Harada (VKH) disease is a bilateral granulomatous panuveitis that can progress to a chronic, relapsing phase. Patients refractory or intolerant to systemic corticosteroids and conventional immunomodulatory therapy pose a major therapeutic challenge, as persistent inflammation can lead to cumulative ocular damage and permanent vision loss. This study assessed the efficacy of tumor necrosis factor-α (TNF-α) inhibitor adalimumab in chronic recurrent VKH disease. Methods: We retrospectively reviewed 16 eyes from 8 patients with chronic recurrent VKH disease who had persistent inflammation despite treatment with corticosteroids and conventional immunomodulatory therapy, and subsequently received adalimumab. Primary outcomes were changes in subfoveal choroidal thickness (SFCT) and systemic corticosteroid dose reduction. Secondary outcomes included visual acuity, inflammatory parameters (anterior chamber cell, flare, and vitreous haze), and central macular thickness (CMT). All outcomes were compared between baseline and 6 months after adalimumab initiation using the Wilcoxon signed-rank test. Results: Mean patient age was 47.6 years and mean follow-up was 31.8 months. SFCT decreased from 326.7 ± 129.1 µm to 231.6 ± 72.9 µm at 6 months (p < 0.001). Systemic steroid dose decreased from 14.7 ± 14.0 mg to 4.1 ± 3.8 mg (p = 0.027). Mean annualized relapse rate decreased from 3.61 to 0.08 episodes/year (p = 0.012). Anterior chamber cell grade decreased from 0.81 ± 0.66 to 0.09 ± 0.20 (p < 0.001). Visual acuity, flare, vitreous haze, and CMT showed no significant change. No serious adverse events occurred. Conclusions: TNF-α inhibition with adalimumab appears effective as steroid-sparing therapy for controlling recurrent inflammation and reducing steroid dependence in patients with chronic recurrent VKH disease refractory to conventional treatment. Full article
(This article belongs to the Special Issue Innovations in Therapeutic Strategies for Retinal and Neurodegenerative Diseases)
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17 pages, 3664 KB  
Article
Neuroprotective Effect of Methylene Blue in a Rat Model of Traumatic Optic Neuropathy
by Nicolás S. Ciranna, Ronan Nakamura, Rafael Peláez, Álvaro Pérez-Sala, Patricia Sarrión, Juan C. Fernández, Alejandra Paganelli, Agustín P. Aranalde, Ulises P. Ruiz, Juan J. López-Costa, César F. Loidl, Alfredo Martínez and Manuel Rey-Funes
Pharmaceuticals 2025, 18(6), 920; https://doi.org/10.3390/ph18060920 - 19 Jun 2025
Cited by 1 | Viewed by 3580
Abstract
Background: Traumatic optic neuropathy (TON) represents a major cause of vision loss worldwide, and treatment options are limited. Here, we study whether methylene blue (MB), a free radical scavenger, is able to prevent morphological and electrophysiological hallmarks of neuropathy in an animal [...] Read more.
Background: Traumatic optic neuropathy (TON) represents a major cause of vision loss worldwide, and treatment options are limited. Here, we study whether methylene blue (MB), a free radical scavenger, is able to prevent morphological and electrophysiological hallmarks of neuropathy in an animal model of TON. Methods: The left eyes of Wistar rats were subjected to intraorbital nerve crush (IONC) while the right ones were sham operated. The group of rats treated with MB (n = 16) received five intraperitoneal injections with 2.0 mg/kg MB in the 24 h following IONC while the control group (n = 16) received just vehicle (PBS) as a control. Twenty-one days after surgery, scotopic full field (scERG), scotopic oscillatory potentials (OP), photopic full field (phERG) and pattern (PERG) electroretinography were performed for retinal function assessment. Furthermore, the number of cell nuclei in the ganglion cell layer (GCL) was recorded in post mortem histological sections. Results: IONC induced very significant reductions in electrophysiological parameters including scotopic a- and b-wave, OPs, photopic b-wave, PhNR amplitude and N2 amplitude. In addition, it also generated a significant prolongation of the N2 implicit time, indicating a profound impact on retinal function. This was further corroborated by a very significant reduction in the number of neuronal nuclei in the GCL, suggesting an intense loss and functional impairment of retinal ganglion cells. MB treatment was able to prevent, partially or completely, all those parameters, indicating the efficiency of such approach. Conclusions: Since MB is already approved for clinical use and presents a high safety profile, it could be repurposed as a neuroprotective drug for ophthalmological applications once proper phase 2 clinical trials are accomplished. Full article
(This article belongs to the Special Issue Innovations in Therapeutic Strategies for Retinal and Neurodegenerative Diseases)
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