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Biomedicines
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Mechanisms and Novel Therapeutic Approaches for Neurodegenerative Diseases (2nd Edition)
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Mechanisms and Novel Therapeutic Approaches for Neurodegenerative Diseases (2nd Edition)

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 2748

Special Issue Editor

Dr. Fernando Cardona

E-Mail Website
Guest Editor
Instituto de Biomedicina de Valencia-CSIC, 46010 Valencia, Spain
Interests: genetics; molecular biology; biochemistry; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are among the most prevalent health problems faced by the elderly. These pathologies generate problems regarding autonomy in those affected, and pose a burden to public health and health systems.

The mechanisms that underlie neurodegeneration are sometimes common to various diseases and differentiated in others. Nonetheless, in many cases, the mechanisms implicated in these diseases are unknown, and if they are known, there are no effective therapies to treat them. In fact, there are few therapies for the treatment of these diseases, or for preventing, slowing or halting neurodegeneration.

In this Special Issue, we invite our colleagues to submit orignal research and review articles that focus on the molecular and cellular mechanisms of neurodegeneration, as well as therapeutic approaches. Manuscripts that address related subjects are also welcome.

Dr. Fernando Cardona
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. Biomedicines 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 2600 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
  • cellular mechanisms
  • molecular mechanisms
  • neurodegeneration models
  • protein misfolding
  • protein aggregation
  • neuronal death
  • molecular therapy
  • cellular therapy
  • therapeutics
  • medical chemistry
  • drug screening

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Related Special Issue

Published Papers (3 papers)

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Research

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17 pages, 5489 KiB  
Article
Relationship Between Brain Insulin Resistance, Carbohydrate Consumption, and Protein Carbonyls, and the Link Between Peripheral Insulin Resistance, Fat Consumption, and Malondialdehyde
by Elena Salazar-Hernández, Oscar Ezequiel Bahena-Cuevas, Juan Miguel Mendoza-Bello, Martha Isela Barragán-Bonilla, Manuel Sánchez-Alavez and Mónica Espinoza-Rojo
Biomedicines 2025, 13(2), 404; https://doi.org/10.3390/biomedicines13020404 - 7 Feb 2025
Viewed by 711
Abstract
The consumption of a high-fat (HFD) or high-carbohydrate/low-fat (LFD) diet is related to insulin resistance; however, central and peripheral alterations can occur independently. In this study, the timeline of insulin resistance was determined while taking into consideration the role of diet in oxidative [...] Read more.
The consumption of a high-fat (HFD) or high-carbohydrate/low-fat (LFD) diet is related to insulin resistance; however, central and peripheral alterations can occur independently. In this study, the timeline of insulin resistance was determined while taking into consideration the role of diet in oxidative damage. Background/Objectives: The aim of this study was to ascertain whether a HFD or LFD induces peripheral insulin resistance (PIR) before brain insulin resistance (BIR), and whether the timing of these alterations correlates with heightened oxidative damage markers in plasma, adipose tissue, and the cerebral cortex. Methodology and Results: Three-month-old C57BL/6 male mice were fed with a HFD, LFD, or standard diet for 1, 2, or 3 months. Glucose and insulin tolerance tests were performed to determine PIR, and the hypothalamic thermogenic response to insulin was used to determine their BIR status. For oxidative damage, the levels of malondialdehyde (MDA) and the protein carbonyl group (PCO) and the enzymatic activity of glutathione peroxidase (GSH-Px) were evaluated in plasma, white adipose tissue, brown adipose tissue, and the cerebral cortex. PIR occurred at 3 months of the HFD, but MDA levels in the white adipose tissue increased at 2 months. BIR occurred at 1 and 2 months of the LFD, but the enzymatic activity of GSH-Px was lower at 1 month and the amount of the PCO increased at 2 months. Conclusions: The intake of a HFD or LFD of different durations can influence the establishment of PIR or BIR, and oxidative damage in the fat tissue and cerebral cortex can play an important role. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Neurodegenerative Diseases (2nd Edition))
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Review

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12 pages, 1949 KiB  
Review
Corneal Neurotization, Recent Progress, and Future Perspectives
by Ovidiu Samoilă, Lăcrămioara Samoilă and Lorina Petrescu
Biomedicines 2025, 13(4), 961; https://doi.org/10.3390/biomedicines13040961 - 14 Apr 2025
Viewed by 311
Abstract
Neurotrophic keratopathy (NK) is a rare degenerative disease caused by impairment of the trigeminal nerve, leading to corneal anesthesia, epithelial breakdown, and progressive vision loss. Conventional treatments primarily focus on symptom management and the prevention of complications, but they do not address the [...] Read more.
Neurotrophic keratopathy (NK) is a rare degenerative disease caused by impairment of the trigeminal nerve, leading to corneal anesthesia, epithelial breakdown, and progressive vision loss. Conventional treatments primarily focus on symptom management and the prevention of complications, but they do not address the underlying nerve dysfunction. Corneal neurotization (NT) has emerged as a promising surgical intervention aimed at restoring corneal sensation and improving ocular surface homeostasis. This review evaluates the outcomes of corneal neurotization in patients with NK and compares the effectiveness of direct (DNT) and indirect (INT) techniques. Studies have reported significant improvements in corneal sensitivity, with success rates ranging from 60.7% to 100% (mean: 90%). Most patients experienced recovery of corneal sensation, as measured by the Cochet–Bonnet aesthesiometer, with no significant differences in outcomes between DNT and INT. Indirect neurotization using a sural nerve graft was the most commonly employed technique (63% of cases), while the use of acellular allografts demonstrated comparable efficacy and simplified the procedure. Postoperative corneal sensitivity increased significantly, from a preoperative average of 2.717 mm to 36.01 mm, with reinnervation typically occurring within 4–6 months and peaking at 12 months. In vivo confocal microscopy confirmed the presence of nerve regeneration. Neurotization was found to be safe, with minimal donor-site complications, which generally resolved within one year. Although the procedure improves corneal sensation and tear film stability, visual acuity outcomes remain variable due to pre-existing corneal damage. Early intervention is, therefore, recommended to prevent irreversible scarring. However, the number of patients undergoing the procedure remains limited, making it difficult to draw definitive conclusions. Most available studies consist of small case series. Further research with larger sample sizes is needed to refine surgical techniques and optimize patient selection, thereby improving outcomes in the management of NK. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Neurodegenerative Diseases (2nd Edition))
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18 pages, 2271 KiB  
Review
Cytokine Signaling in Diabetic Neuropathy: A Key Player in Peripheral Nerve Damage
by Zahra Nashtahosseini, Majid Eslami, Elham Paraandavaji, Alireza Haraj, Bahram Fadaee Dowlat, Ehsan Hosseinzadeh, Valentyn Oksenych and Ramtin Naderian
Biomedicines 2025, 13(3), 589; https://doi.org/10.3390/biomedicines13030589 - 28 Feb 2025
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Abstract
Diabetic peripheral neuropathy (DPN) is a debilitating complication of diabetes mellitus, characterized by progressive nerve damage driven by chronic hyperglycemia and systemic inflammation. The pathophysiology of DPN is significantly influenced by pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α. These cytokines promote oxidative [...] Read more.
Diabetic peripheral neuropathy (DPN) is a debilitating complication of diabetes mellitus, characterized by progressive nerve damage driven by chronic hyperglycemia and systemic inflammation. The pathophysiology of DPN is significantly influenced by pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α. These cytokines promote oxidative stress, vascular dysfunction, and neuronal degeneration by activating important signaling pathways including NF-κB and MAPK. While IL-6 promotes a pro-inflammatory microenvironment, increasing neuronal damage and neuropathic pain, TNF-α and IL-1β worsen Schwann cell failure by compromising axonal support and causing demyelination. Immune cell infiltration and TLR activation increase the inflammatory cascade in DPN, resulting in a persistent neuroinflammatory state that sustains peripheral nerve injury. The main characteristics of DPN are axonal degeneration, decreased neurotrophic support, and Schwann cell dysfunction, which weaken nerve transmission and increase susceptibility to damage. Advanced glycation end-products, TNF-α, and CXCL10 are examples of biomarkers that may be used for early diagnosis and disease progression monitoring. Additionally, crucial molecular targets have been found using proteomic and transcriptome techniques, enabling precision medicine for the treatment of DPN. This review emphasizes the importance of cytokine signaling in the pathogenesis of DPN and how cytokine-targeted treatments might reduce inflammation, restore nerve function, and improve clinical outcomes for diabetic patients. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Neurodegenerative Diseases (2nd Edition))
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