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Neurodegenerative Retinal Diseases and Other Neurodegenerative Pathologies
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Neurodegenerative Retinal Diseases and Other Neurodegenerative Pathologies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (20 April 2024) | Viewed by 3350

Special Issue Editors

Dr. Salvador Pastor-Idoate

E-Mail Website
Guest Editor
1. Department of Ophthalmology Hospital Clínico Universitario of Valladolid, Valladolid, Spain
2. Retina Group, IOBA-Eye Institute, University of Valladolid, Valladolid, Spain
Interests: OCT; ophthalmology
Dr. Ricardo Usategui-Martín

E-Mail Website
Guest Editor
Cell Biology, Faculty of Medicine, University of Valladolid, Valladolid, Spain
Interests: molecular and cell biology; bone; genetic; neuron; retina
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is our pleasure to inform you about the Special Issue, “New Discoveries in Neurodegenerative Retinal Diseases and Other Neurodegenerative Pathologies, and Molecular Therapies”. Neurodegenerative pathologies including neurodegenerative retinal diseases constitute a worldwide major public health burden. Neurodegenerative diseases are a broad spectrum of clinically different pathologies that share some molecular characteristics. They are multifactorial alterations in which molecular, genetic, and environmental factors are crucial. It is important to understand the molecular mechanisms involved in their appearance, which then allows for therapeutic targets to be established. An increased knowledge of their pathophysiology allows for a better understanding of the diseases and their solutions. Moreover, knowledge on these new therapeutic targets will allow for the design of new therapeutic options. In this scenario, this Special Issue focuses on molecular factors associated with the pathogenesis of neurodegenerative retinal diseases and other neurodegenerative pathologies. It will be published in the International Journal of Molecular Sciences (IJMS, https://www.mdpi.com/journal/ijms, ISSN 1422-0067). We invite researchers to submit original research or review articles on basic, translational, and clinical aspects that describe new concepts associated with neurodegenerative retinal diseases and other neurodegenerative pathologies.

Dr. Salvador Pastor-Idoate
Dr. Ricardo Usategui-Martin
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • neurodegeneration
  • retina
  • molecular biology
  • genetics and cellular biology

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Published Papers (2 papers)

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Research

15 pages, 4157 KiB  
Article
Microcurrent Therapy Mitigates Neuronal Damage and Cognitive Decline in an Alzheimer’s Disease Mouse Model: Insights into Mechanisms and Therapeutic Potential
by Eun Ho Kim, Won Seok Lee and Dong Rak Kwon
Int. J. Mol. Sci. 2024, 25(11), 6088; https://doi.org/10.3390/ijms25116088 - 31 May 2024
Cited by 1 | Viewed by 1044
Abstract
Alzheimer’s disease (AD) presents a significant challenge due to its multifaceted nature, characterized by cognitive decline, memory loss, and neuroinflammation. Though AD is an extensively researched topic, effective pharmacological interventions remain elusive, prompting explorations into non-pharmacological approaches. Microcurrent (MC) therapy, which utilizes imperceptible [...] Read more.
Alzheimer’s disease (AD) presents a significant challenge due to its multifaceted nature, characterized by cognitive decline, memory loss, and neuroinflammation. Though AD is an extensively researched topic, effective pharmacological interventions remain elusive, prompting explorations into non-pharmacological approaches. Microcurrent (MC) therapy, which utilizes imperceptible currents, has emerged as a potent clinical protocol. While previous studies have focused on its therapeutic effects, this study investigates the impact of MC on neuronal damage and neuroinflammation in an AD mouse model, specifically addressing potential side effects. Utilizing 5xFAD transgenic mice, we examined the effects of MC therapy on neuronal integrity and inflammation. Our findings suggest that MC therapy attenuates memory impairment and reduces neurodegeneration, as evidenced by improved performance in memory tests and the preservation of the neuronal structure. Additionally, MC therapy significantly decreases amyloid-beta (Aβ) plaque deposition and inhibits apoptosis, indicating its potential to mitigate AD pathology. This study determined that glial activation is effectively reduced by using MC therapy to suppress the TLR4-MyD88-NFκB pathway, which consequently causes the levels of inflammatory factors TNF-α, IL-1β, and IL-6 to decrease, thus implicating TLR4 in neurodegenerative disease-related neuroinflammation. Furthermore, while our study did not observe significant adverse effects, a further clinical trial into potential side effects and neuroinflammatory responses associated with MC therapy is warranted. Full article
(This article belongs to the Special Issue Neurodegenerative Retinal Diseases and Other Neurodegenerative Pathologies)
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22 pages, 4226 KiB  
Article
Identification of 7-Ketocholesterol-Modulated Pathways and Sterculic Acid Protective Effect in Retinal Pigmented Epithelium Cells by Using Genome-Wide Transcriptomic Analysis
by Ana Pariente, Álvaro Pérez-Sala, Rodrigo Ochoa, Miriam Bobadilla, Ángela Villanueva-Martínez, Rafael Peláez and Ignacio M. Larráyoz
Int. J. Mol. Sci. 2023, 24(8), 7459; https://doi.org/10.3390/ijms24087459 - 18 Apr 2023
Cited by 3 | Viewed by 1729
Abstract
Age-related macular degeneration (AMD) is the leading cause of blindness in developed countries. AMD is characterized by the formation of lipidic deposits between the retinal pigment epithelium (RPE) and the choroid called drusen. 7-Ketocholesterol (7KCh), an oxidized-cholesterol derivative, is closely related to AMD [...] Read more.
Age-related macular degeneration (AMD) is the leading cause of blindness in developed countries. AMD is characterized by the formation of lipidic deposits between the retinal pigment epithelium (RPE) and the choroid called drusen. 7-Ketocholesterol (7KCh), an oxidized-cholesterol derivative, is closely related to AMD as it is one of the main molecules accumulated in drusen. 7KCh induces inflammatory and cytotoxic responses in different cell types, and a better knowledge of the signaling pathways involved in its response would provide a new perspective on the molecular mechanisms that lead to the development of AMD. Furthermore, currently used therapies for AMD are not efficient enough. Sterculic acid (SA) attenuates the 7KCh response in RPE cells and is presented as an alternative to improve these therapies. By using genome-wide transcriptomic analysis in monkey RPE cells, we have provided new insight into 7KCh-induced signaling in RPE cells, as well as the protective capacity of SA. 7KCh modulates the expression of several genes associated with lipid metabolism, endoplasmic reticulum stress, inflammation and cell death and induces a complex response in RPE cells. The addition of SA successfully attenuates the deleterious effect of 7KCh and highlights its potential for the treatment of AMD. Full article
(This article belongs to the Special Issue Neurodegenerative Retinal Diseases and Other Neurodegenerative Pathologies)
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