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

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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 1248

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Dr. Fernando Cardona

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Instituto de Biomedicina de Valencia-CSIC, 46010 Valencia, Spain
Interests: genetics; molecular biology; biochemistry; neurodegenerative diseases
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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

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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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Mechanisms and Novel Therapeutic Approaches for Neurodegenerative Diseases in Biomedicines (7 articles)

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Research

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17 pages, 5489 KiB

Open AccessArticle

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

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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 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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Figure 1

Figure 1
Experimental diagram of obesity induction and measurement of peripheral and cerebral insulin resistance in C57BL/6 mice. Mice were exposed to standard, low-fat, or high-fat diets for 1 (4 weeks), 2 (8 weeks), and 3 (12 weeks) months (MO). Body weight was measured weekly until 12 weeks. Device implant was performed at weeks 2 (1 MO group), 5 (2 MO group), and 9 (3 MO group). Subsequently, the insulin tolerance test (ITT) and the glucose tolerance test (GTT) were performed at weeks 2, 6, and 10. Placement of the guide cannula for insulin injections in the mice was performed through stereotaxic surgery at weeks 3, 7, and 11. Finally, the mice were sacrificed at weeks 4, 8, and 12 to obtain organs and determine oxidative damage markers. Full article ">Figure 2
Effect of fat intake on body weight of C57BL/6 mice. Body weight of mice fed different diets for 1 (A), 2 (B), and 3 (C) months (MO) are shown. Data are shown as the mean ± standard deviation. Statistical significance using two-way analysis of variance (ANOVA) followed by Student’s t-test. C: standard diet (black circle); LFD: low-fat diet or high-carbohydrate diet (light-gray square); HFD: high-fat diet (strong gray triangle). The solid arrow indicates the time of performance of the laparotomy and the dotted arrow indicates the time of performance of stereotaxic surgery. C vs. LFD = + p < 0.05, C vs. HFD * p < 0.05, ** p < 0.01, and *** p < 0.001. Full article ">Figure 3
Effect of HFD and LFD intake on glucose tolerance and peripheral insulin sensitivity in C57BL/6 mice. Glucose levels are shown versus time (0, 30, 60, 60, 90, and 120 min) after administration of 2 g glucose/kg body weight in mice fed for 2 (A), 6 (B), and 10 (C) weeks on low-fat or high-carbohydrate diet (LFD), high-fat (HFD), or standard diet (C) and the area under the curve (AUC) (D) for the glucose tolerance test (GTT) for the 1, 2, and 3 month (MO) groups. Glucose levels are shown versus time (0, 30, 60, 60, 90, and 120 min) after administration of 0.5 IU insulin/kg body weight intraperitoneally in LFD, HFD, or C mice fed for 2 (E), 6 (F), and 10 (G) weeks and the AUC (H) for the insulin tolerance test (ITT) for the 1, 2, and 3 MO groups. Data are shown as the mean ± standard deviation. + p < 0.05, ++ p < 0.01 significance LFD vs. C. * p < 0.05, ** p < 0.01, *** p < 0.001 significance HFD vs. C. Full article ">Figure 4
Effect of brain insulin injections on core body temperature in C57BL/6 mice. Changes in core body temperature (CBT) over 4 h after local injection of insulin (0.015, 0.03, and 0.06 IU) and vehicle in the POA by groups of 1 (A–D), 2 (E–H), and 3 (I–L)months (MO) of exposure to the diets. Data are shown as the mean ± standard deviation. * p < 0.05, ** p < 0.01 significance vs. C. C: standard diet (black circle); LFD: low-fat diet or high-carbohydrate diet (orange square); HFD: high-fat diet (blue triangle). The orange arrow indicates insulin injection time. Full article ">Figure 5
Oxidative damage in plasma, white adipose tissue, brown adipose tissue, and cerebral cortex. Percentage of malondialdehyde (MDA) (A,D,G,J), protein carbonyl group (PCO) (B,E,H,K), and glutathione peroxidase activity (GSH-Px) (C,F,I,L) in plasma, white adipose tissue, brown adipose tissue, and cerebral cortex of mice fed a standard diet (C), low-fat diet (LFD), and high-fat diet (HFD) for 1, 2, and 3 months (MO). Data are shown as the mean ± standard deviation. Statistical significance with two-way analysis of variance (ANOVA) followed by Student’s t-test. * p < 0.05; ** p < 0.01. Full article ">

Review

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18 pages, 2271 KiB

Open AccessReview

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

Viewed by 173

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 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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Figure 1
Disruption of cytokine regulation under chronic hyperglycemia conditions. Chronic hyperglycemia triggers NLRP3 activation, ROS generation, and AGEs accumulation, leading to activation of inflammatory pathways, including MAPK, NF-κB, and p38. These pathways promote the release of pro-inflammatory cytokines such as IL-6, IL-8, IL-17, IL-1β, and IL-18, contributing to systemic inflammation and diabetic complications such as neuropathy. The figure also shows the disruption of cytokine regulation in diabetes. Chronic hyperglycemia drives oxidative stress and NLRP3 inflammasome activation, leading to IL-6, IL-8, IL-17, and TGF-β upregulation through NF-κB, MAPK, and PKC pathways, amplifying inflammatory responses. Full article ">Figure 2
Cytokine signaling pathways in inflammation regulation. Pro-inflammatory cytokines (IL-6, TNF-α, IL-17, etc.) activate NF-κB, MAPK, and JAK/STAT pathways to drive inflammation, while anti-inflammatory cytokines (IL-10, IL-4, TGF-β) suppress inflammation through JAK/STAT and SMAD pathways. Adapted from cytokine mechanisms discussed in inflammatory neuropathies. Full article ">Figure 3
Therapeutic implications of targeting cytokine signaling in diabetic neuropathy. Current therapies and novel approaches aim to modulate cytokines (TNF-α, RANTES, sVCAM-1) and reduce oxidative stress to alleviate neuropathic pain, improve nerve function, and reduce inflammation. Full article ">Figure 4
Emerging biomarkers and therapeutic advances in diabetic neuropathy. Early detection biomarkers (adiponectin, CXCL10, AGEs) and cytokine-related markers (IL-6, TNF-α, IL-10) facilitate disease monitoring. Proteomics and transcriptomics uncover novel therapeutic targets such as CQYG therapy and HSP90 inhibitors, paving the way for precision medicine approaches. Full article ">

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