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Challenges and Innovation in Neurodegenerative Diseases, 2nd Edition
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Challenges and Innovation in Neurodegenerative Diseases, 2nd Edition

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: 20 July 2025 | Viewed by 2800

Special Issue Editor

Dr. King-Ho Cheung

E-Mail Website
Guest Editor
School of Chinese Medicine, Hong Kong Baptist University, 7 Baptist University Road, Kowloon Tong, Kowloon, Hong Kong, China
Interests: ion channels; electrophysiology; epithelial transport; Alzheimer’s disease; neurodegenerative diseases; new drug development
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The umbrella of neurodegeneration covers a group of heterogeneous diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and others that account for more than 5% of the global burden of all diseases. Although considerable advances in understanding the triggers of neurodegenerative diseases have led to the development of new drugs, there are a handful of challenges that remain in the field that we must overcome to allow for cures to these diseases. For example, good disease models that more faithfully recapitulate human disease are urgently needed. A full understanding of the involvement of protein aggregation in disease progression and the identification of disease-specific biomarkers would allow the early detection of neurodegeneration and permit reliable disease progression monitoring. The recent application of machine learning and artificial intelligence in new drug discovery and development from natural products, as well as the use of stem cell therapy, also brings hope to patients with neurodegenerative diseases.

This Special Issue aims to collect views on the current challenges in the field, the exciting progress in deciphering the disease pathogenesis, and the cutting-edge technologies for the early detection of neurodegeneration. The accumulation of innovative findings in these areas may pave the way for the development of therapeutic interventions for neurogenerative diseases.

Dr. King-Ho Cheung
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • neurodegenerative diseases
  • pathogenesis
  • biomarkers
  • disease model
  • natural product
  • new drug discovery
  • therapy
  • machine learning
  • stem cell therapy

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Related Special Issue

Published Papers (4 papers)

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Research

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29 pages, 4801 KiB  
Article
Non-Categorical Analyses Identify Rotenone-Induced ‘Parkinsonian’ Rats Benefiting from Nano-Emulsified Punicic Acid (Nano-PSO) in a Phenotypically Diverse Population: Implications for Translational Neurodegenerative Therapies
by Jennifer Viridiana Sánchez-Camacho, Margarita Gómez-Chavarín, Nuria Galindo-Solano, Patricia Padilla-Cortés, José Luis Maldonado-García, Gilberto Pérez-Sánchez, Lenin Pavón, Jesús Ramírez-Santos, Gabriel Roldán Roldán, Modesto Gómez-López and Gabriel Gutierrez-Ospina
Int. J. Mol. Sci. 2024, 25(23), 12635; https://doi.org/10.3390/ijms252312635 - 25 Nov 2024
Viewed by 637
Abstract
The pursuit of nutraceuticals to improve the quality of life for patients with neurodegenerative conditions is a dynamic field within neuropharmacology. Unfortunately, many nutraceuticals that show promise in preclinical studies fail to demonstrate significant clinical benefits in human trials, leading to their exclusion [...] Read more.
The pursuit of nutraceuticals to improve the quality of life for patients with neurodegenerative conditions is a dynamic field within neuropharmacology. Unfortunately, many nutraceuticals that show promise in preclinical studies fail to demonstrate significant clinical benefits in human trials, leading to their exclusion as therapeutic options. This discrepancy may stem from the categorical interpretation of preclinical and clinical results. Basic researchers often assume that non-human experimental animals exhibit less phenotypic variability than humans. This belief overlooks interindividual phenotype variation, thereby leading to categorical conclusions being drawn from experiments. Consequently, when human clinical trials are conducted, the researchers expect similarly conclusive results. If these results are not achieved, the nutraceutical is deemed ineffective for clinical use, even if numerous individuals might benefit. In our study, we evaluated whether analyzing phenotype variability and similarity through non-categorical methods could help identify rotenone (ROT)-treated rats that might benefit from consuming nano-emulsified punicic acid (Nano-PSO), even if the prevention of “parkinsonism” or the restoration of neurometabolic function is inconsistent across individuals. Our findings supported this hypothesis. The benefits of Nano-PSO were not categorical; however, analyzing phenotype variance allowed us to identify ROT rats with varying degrees of benefit from Nano-PSO consumption. Hence, the translational potential of results from basic science studies testing nutraceuticals as pharmaceutical products against neurodegeneration may improve if researchers also interpret their results using non-categorical methods of data analysis for population screening, even if the overall therapeutic outcomes for the entire population show internal inconsistencies. Full article
(This article belongs to the Special Issue Challenges and Innovation in Neurodegenerative Diseases, 2nd Edition)
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12 pages, 1174 KiB  
Article
α-Synuclein Oligomers in Skin Biopsies Predict the Worsening of Cognitive Functions in Parkinson’s Disease: A Single-Center Longitudinal Cohort Study
by Elena Contaldi, Milo Jarno Basellini, Samanta Mazzetti, Alessandra Maria Calogero, Aurora Colombo, Viviana Cereda, Gionata Innocenti, Valentina Ferri, Daniela Calandrella, Ioannis U. Isaias, Gianni Pezzoli and Graziella Cappelletti
Int. J. Mol. Sci. 2024, 25(22), 12176; https://doi.org/10.3390/ijms252212176 - 13 Nov 2024
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Abstract
α-synuclein oligomers within synaptic terminals of autonomic fibers of the skin reliably discriminate Parkinson’s disease (PD) patients from healthy controls. Nonetheless, the prognostic role of oligomers for disease progression is unknown. We explored whether α-synuclein oligomers evaluated as proximity ligation assay (PLA) score [...] Read more.
α-synuclein oligomers within synaptic terminals of autonomic fibers of the skin reliably discriminate Parkinson’s disease (PD) patients from healthy controls. Nonetheless, the prognostic role of oligomers for disease progression is unknown. We explored whether α-synuclein oligomers evaluated as proximity ligation assay (PLA) score may predict the worsening of cognitive functions in patients with Parkinson’s disease. Thirty-four patients with PD and thirty-four healthy controls (HC), matched 1:1 for age and sex, were enrolled. Patients with PD underwent baseline skin biopsy and an assessment of cognitive domains including Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Clock Drawing Test, and Frontal Assessment Battery. At the last follow-up visit available, patients were either cognitively stable (PD-CS) or cognitively deteriorated (PD-CD). α-synuclein oligomers were quantified as PLA scores. Differences between groups were assessed, controlling for potential confounders. The relationship between skin biopsy measures and cognitive changes was explored using correlation and multivariable regression analyses. The discrimination power of the PLA score was assessed via ROC curve. To elucidate the relationship between skin biopsy and longitudinal cognitive measures, we conducted multivariable regression analyses using delta scores of cognitive tests (Δ) as dependent variables. We found that PD-CD had higher baseline PLA scores than PD-CS (p = 0.0003), and they were correctly identified in the ROC curve analysis (AUC = 0.872, p = 0.0003). Furthermore, ANCOVA analysis with Bonferroni correction, considering all groups (PD-CS, PD-CD, and HC), showed significant differences between PD-CS and PD-CD (p = 0.003), PD-CS and HC (p = 0.002), and PD-CD and HC (p < 0.001). In the regression model using ΔMMSE as the dependent variable, the PLA score was found to be a significant predictor (β = −0.441, p = 0.016). Similar results were observed when evaluating the model with ΔMoCA (β = −0.378, p = 0.042). In conclusion, patients with Parkinson’s disease with higher α-synuclein burden in the peripheral nervous system may be more susceptible to cognitive decline. Full article
(This article belongs to the Special Issue Challenges and Innovation in Neurodegenerative Diseases, 2nd Edition)
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20 pages, 4004 KiB  
Article
Regulatory Peptide Pro-Gly-Pro Accelerates Neuroregeneration of Primary Neuroglial Culture after Mechanical Injury in Scratch Test
by Zanda Bakaeva, Mikhail Goncharov, Fyodor Frolov, Irina Krasilnikova, Elena Sorokina, Arina Zgodova, Elena Smolyarchuk, Sergey Zavadskiy, Liudmila Andreeva, Nikolai Myasoedov, Andrey Fisenko and Kirill Savostyanov
Int. J. Mol. Sci. 2024, 25(20), 10886; https://doi.org/10.3390/ijms252010886 - 10 Oct 2024
Viewed by 1012
Abstract
The scratch test is used as an experimental in vitro model of mechanical damage to primary neuronal cultures to study the mechanisms of cell death in damaged areas. The involvement of NMDA receptors in processes leading to delayed neuronal death, due to calcium [...] Read more.
The scratch test is used as an experimental in vitro model of mechanical damage to primary neuronal cultures to study the mechanisms of cell death in damaged areas. The involvement of NMDA receptors in processes leading to delayed neuronal death, due to calcium dysregulation and synchronous mitochondrial depolarization, has been previously demonstrated. In this study, we explored the neuroregenerative potential of Pro-Gly-Pro (PGP)—an endogenous regulatory peptide with neuroprotective and anti-inflammatory properties and a mild chemoattractant effect. Mechanical injury to the primary neuroglial culture in the form of a scratch caused acute disruption of calcium homeostasis and mitochondrial functions. This was accompanied by neuronal death alongside changes in the profile of neuronal markers (BDNF, NSE and GFAP). In another series of experiments, under subtoxic doses of glutamate (Glu, 33 μM), delayed changes in [Ca2+]i and ΔΨm, i.e., several days after scratch application, were more pronounced in cells in damaged neuroglial cultures. The percentage of cells that restored the initial level of [Ca2+]i (p < 0.05) and the rate of recovery of ΔΨm (p < 0.01) were decreased compared with undamaged cells. Prophylactic application of PGP (100 μM, once) prevented the increase in [Ca2+]i and the sharp drop in mitochondrial potential [ΔΨm] at the time of scratching. Treatment with PGP (30 μM, three or six days) reduced the delayed Glu-induced disturbances in calcium homeostasis and cell death. In the post-glutamate period, the surviving neurons more effectively restored the initial levels of [Ca2+]i (p < 0.001) and Ψm (p < 0.0001). PGP also increased intracellular levels of BDNF and reduced extracellular NSE. In the context of the peptide’s therapeutic effect, the recovery of the damaged neuronal network occurred faster due to reduced astrogliosis and increased migration of neurons to the scratch area. Thus, the peptide PGP has a neuroprotective effect, increasing the survival of neuroglial cells after mechanical trauma in vitro by reducing cellular calcium overload and preventing mitochondrial dysfunction. Additionally, the tripeptide limits the post-traumatic consequences of mechanical damage: it reduces astrogliosis and promotes neuronal regeneration. Full article
(This article belongs to the Special Issue Challenges and Innovation in Neurodegenerative Diseases, 2nd Edition)
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Review

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21 pages, 893 KiB  
Review
Selenoproteins: Zoom-In to Their Metal-Binding Properties in Neurodegenerative Diseases
by Carmen Duță, Corina Muscurel, Carmen Beatrice Dogaru and Irina Stoian
Int. J. Mol. Sci. 2025, 26(3), 1305; https://doi.org/10.3390/ijms26031305 (registering DOI) - 3 Feb 2025
Abstract
Selenoproteins contain selenium (Se), which is included in the 21st proteinogenic amino acid selenocysteine (Sec). Selenium (Se) is an essential trace element that exerts its biological actions mainly through selenoproteins. Selenoproteins have crucial roles in maintaining healthy brain activity. At the same time, [...] Read more.
Selenoproteins contain selenium (Se), which is included in the 21st proteinogenic amino acid selenocysteine (Sec). Selenium (Se) is an essential trace element that exerts its biological actions mainly through selenoproteins. Selenoproteins have crucial roles in maintaining healthy brain activity. At the same time, brain-function-associated selenoproteins may also be involved in neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). The selenoproteins GPx4 (glutathione peroxidase 4), GPx1 (glutathione peroxidase 1), SELENOP (selenoprotein P), SELENOK (selenoprotein K), SELENOS (selenoprotein S), SELENOW (selenoprotein W), and SELENOT (selenoprotein T) are highly expressed, specifically in AD-related brain regions being closely correlated to brain function. Only a few selenoproteins, mentioned above (especially SELENOP), can bind transition and heavy metals. Metal ion homeostasis accomplishes the vital physiological function of the brain. Dyshomeostasis of these metals induces and entertains neurodegenerative diseases. In this review, we described some of the proposed and established mechanisms underlying the actions and properties of the above-mentioned selenoproteins having the characteristic feature of binding transition or heavy metals. Full article
(This article belongs to the Special Issue Challenges and Innovation in Neurodegenerative Diseases, 2nd Edition)
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