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Advances in Neurodegenerative Diseases Research and Therapy—Third Edition
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Advances in Neurodegenerative Diseases Research and Therapy—Third 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 August 2025 | Viewed by 11897

Special Issue Editor

Dr. Sumonto Mitra

E-Mail Website
Guest Editor
Division of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institute, 14183 Huddinge, Sweden
Interests: nerve growth factor; neurotrophins; Alzheimer’s disease; therapy; encapsulated cell biodelivery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Degenerative diseases of the nervous system affect millions of people worldwide and have limited therapeutic interventions available presently since the blood–brain barrier restricts the passage of most drug candidates into the brain tissue. The term ‘neurodegenerative disease’ is often used as an umbrella term which includes various debilitating conditions which affect the brain, including Alzheimer’s, Parkinson’s, Huntington’s diseases, etc. Previous studies have focused on neuronal degeneration as the primary cause of these diseases, but recent evidence points towards the contribution of glial cells in maintaining a physiological and functioning neural output. Although these diseases have different pathological markers and clinical symptoms, they share common molecular pathways, including gliosis, proteostasis, inflammation, metabolic alterations, etc. It has been evident that understanding the molecular changes occurring during the development and progression of neurodegenerative diseases may lead to the development of effective therapeutic interventions.

This Special Issue, entitled ‘Advances in Neurodegenerative Diseases Research and Therapy—Third Edition’, continues to invite the submission of original research and review articles to provide the latest update on the molecular changes associated with neurodegenerative diseases. Special focus is also on the development of ‘clinically relevant’ therapeutic strategies against neurodegenerative diseases (including optimization studies, clinical efficacy studies, biomarker evaluation, drug delivery, etc.).

Dr. Sumonto Mitra
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
  • therapy
  • molecular mechanisms
  • neuron
  • astrocytes
  • microglia
  • inflammation
  • brain
  • drug delivery

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Related Special Issue

Published Papers (7 papers)

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Research

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25 pages, 2888 KiB  
Article
Steady Moderate Exercise Confers Resilience Against Neurodegeneration and Neuroinflammation in a Mouse Model of Parkinson’s Disease
by Ewelina Palasz, Anna Gasiorowska-Bien, Patrycja Drapich, Wiktor Niewiadomski and Grazyna Niewiadomska
Int. J. Mol. Sci. 2025, 26(3), 1146; https://doi.org/10.3390/ijms26031146 - 28 Jan 2025
Cited by 1 | Viewed by 884
Abstract
Intensive aerobic exercise slows the progression of movement disorders in Parkinson’s disease (PD) and is therefore recommended as an important component of treatment for PD patients. Studies in animal models of PD have shown that vigorous exercise has neuroprotective effects, and emerging evidence [...] Read more.
Intensive aerobic exercise slows the progression of movement disorders in Parkinson’s disease (PD) and is therefore recommended as an important component of treatment for PD patients. Studies in animal models of PD have shown that vigorous exercise has neuroprotective effects, and emerging evidence suggests that it may be a disease-modifying treatment in humans. However, many people with PD may not be able to participate in vigorous exercise because of multiple medical conditions that severely limit their physical activity. In this study, we have shown that chronic MPTP treatment in sedentary mice resulted in loss of dopaminergic neurons in the SNpc, decreased levels of neurotrophins, BDNF and GDNF, and increased levels of inflammatory markers and pro-inflammatory changes in immunocompetent cells. Moderate exercise, initiated both before and after chronic MPTP treatment, significantly attenuated the loss of dopaminergic neurons and increased BDNF and GDNF levels even above those in sedentary control mice. No signs of inflammation were observed in MPTP-treated mice, either when training began before or after MPTP treatment. Training induced beneficial changes in the dopaminergic system, increased levels of neurotrophins and suppression of inflammation were similar for both steady moderate (present data) and intense training (our previously published data). This suggests that there is a kind of saturation when the percentage of rescued dopaminergic neurons reaches the highest possible value, and therefore further increases in exercise intensity do not enhance neuroprotection. In conclusion, our present results compared with the previous data show that increasing exercise intensity beyond the level used in this study does not increase the neuroprotective effect of aerobic training in a mouse model of Parkinson’s disease. Full article
(This article belongs to the Special Issue Advances in Neurodegenerative Diseases Research and Therapy—Third Edition)
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13 pages, 2359 KiB  
Article
Endoplasmic Reticulum Proteins Impact Penetrance in a Pink1-Mutant Drosophila Model
by Melissa Vos, Fabian Ott, Hawwi Gillo, Giuliana Cesare, Sophie Misera, Hauke Busch and Christine Klein
Int. J. Mol. Sci. 2025, 26(3), 979; https://doi.org/10.3390/ijms26030979 - 24 Jan 2025
Viewed by 701
Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder with a high variability of age at onset, disease severity, and progression. This suggests that other factors, including genetic, environmental, or biological factors, are at play in PD. The loss of PINK1 causes a recessive form [...] Read more.
Parkinson’s disease (PD) is a neurodegenerative disorder with a high variability of age at onset, disease severity, and progression. This suggests that other factors, including genetic, environmental, or biological factors, are at play in PD. The loss of PINK1 causes a recessive form of PD and is typically fully penetrant; however, it features a wide range in disease onset, further supporting the existence of protective factors, endogenous or exogenous, to play a role. The loss of Pink1 in Drosophila melanogaster results in locomotion deficits, also observed in PINK1-related PD in humans. In flies, Pink1 deficiency induces defects in the ability to fly; nonetheless, around ten percent of the mutant flies are still capable of flying, indicating that advantageous factors affecting penetrance also exist in flies. Here, we aimed to identify the mechanisms underlying this reduced penetrance in Pink1-deficient flies. We performed genetic screening in pink1-mutant flies to identify RNA expression alterations affecting the flying ability. The most important biological processes involved were transcriptional and translational activities, endoplasmic reticulum (ER) regulation, and flagellated movement and microtubule organization. We validated two ER-related proteins, zonda and windbeutel, to positively affect the flying ability of Pink1-deficient flies. Thus, our data suggest that these processes are involved in the reduced penetrance and that influencing them may be beneficial for Pink1 deficiency. Full article
(This article belongs to the Special Issue Advances in Neurodegenerative Diseases Research and Therapy—Third Edition)
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16 pages, 9076 KiB  
Article
Morphometric Similarity Patterning of Amyloid-β and Tau Proteins Correlates with Transcriptomics in the Alzheimer’s Disease Continuum
by Lorenza Brusini, Giorgio Dolci, Lorenzo Pini, Federica Cruciani, Fabrizio Pizzagalli, Paolo Provero, Gloria Menegaz and Ilaria Boscolo Galazzo
Int. J. Mol. Sci. 2024, 25(23), 12871; https://doi.org/10.3390/ijms252312871 - 29 Nov 2024
Viewed by 925
Abstract
Bridging the gap between cortical morphometric remodeling and gene expression can help to clarify the effects of the selective brain accumulation of Amyloid-β (Aβ) and tau proteins occurring in the Alzheimer’s disease (AD). To this aim, we derived morphometric similarity [...] Read more.
Bridging the gap between cortical morphometric remodeling and gene expression can help to clarify the effects of the selective brain accumulation of Amyloid-β (Aβ) and tau proteins occurring in the Alzheimer’s disease (AD). To this aim, we derived morphometric similarity (MS) networks from 126 Aβ- and tau-positive (Aβ+/tau+) and 172 Aβ−/tau− subjects, and we investigated the association between group-wise regional MS differences and transcriptional correlates thanks to an imaging transcriptomics approach grounded in the Allen Human Brain Atlas (AHBA). The expressed gene with the highest correlation with MS alterations was BCHE, a gene related to Aβ homeostasis. In addition, notably, among the most promising results derived from the enrichment analysis, we found the immune response to be a biological process and astrocytes, microglia, and oligodendrocyte precursors for the cell types. In summary, by relating cortical MS and AHBA-derived transcriptomics, we were able to retrieve findings suggesting the biological mechanisms underlying the Aβ- and tau- induced cortical MS alterations in the AD continuum. Full article
(This article belongs to the Special Issue Advances in Neurodegenerative Diseases Research and Therapy—Third Edition)
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17 pages, 4023 KiB  
Article
Investigating the Impact of the Parkinson’s-Associated GBA1 E326K Mutation on β-Glucocerebrosidase Dimerization and Interactome Dynamics Through an In Silico Approach
by Davide Pietrafesa, Alessia Casamassa, Barbara Benassi, Massimo Santoro, Massimo Marano, Claudia Consales, Jessica Rosati and Caterina Arcangeli
Int. J. Mol. Sci. 2024, 25(21), 11443; https://doi.org/10.3390/ijms252111443 - 24 Oct 2024
Viewed by 5987
Abstract
Heterozygous mutations or genetic variants in the GBA1 gene, which encodes for the β-glucocerebrosidase (GCase), a lysosomal hydrolase enzyme, may increase the risk of Parkinson’s disease (PD) onset. The heterozygous E326K form is one of the most common genetic risk factors for PD [...] Read more.
Heterozygous mutations or genetic variants in the GBA1 gene, which encodes for the β-glucocerebrosidase (GCase), a lysosomal hydrolase enzyme, may increase the risk of Parkinson’s disease (PD) onset. The heterozygous E326K form is one of the most common genetic risk factors for PD worldwide, but, to date, the underlying molecular mechanisms remain unclear. Here, we investigate the effect of the E326K on the structure, stability, dimerization process, and interaction mode with some proteins of the interactome of GCase using multiple molecular dynamics (MD) simulations at pH 5.5 and pH 7.0 to mimic the lysosomal and endoplasmic reticulum environments, respectively. The analysis of the MD trajectories highlights that the E326K mutation did not significantly alter the structural conformation of the catalytic dyad but significantly makes the structure of the dimeric complexes unstable, especially at lysosomal pH, potentially impacting the organization of the quaternary structure. Furthermore, the E326K mutation significantly impacts protein interactions by altering the binding mode with the activator Saposin C (SapC), reducing the binding affinity with the inhibitor α-Synuclein (α-Syn), and increasing the affinity for the Lysosomal integral membrane protein-2 (LIMP-2) transporter. Full article
(This article belongs to the Special Issue Advances in Neurodegenerative Diseases Research and Therapy—Third Edition)
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Review

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24 pages, 1398 KiB  
Review
Role of the Intestinal Microbiota in the Molecular Pathogenesis of Atypical Parkinsonian Syndromes
by Dominika Przewodowska, Piotr Alster and Natalia Madetko-Alster
Int. J. Mol. Sci. 2025, 26(9), 3928; https://doi.org/10.3390/ijms26093928 - 22 Apr 2025
Viewed by 245
Abstract
The role of the intestinal microbiota and its influence on neurodegenerative disorders has recently been extensively explored, especially in the context of Parkinson’s disease (PD). In particular, its role in immunomodulation, impact on inflammation, and participation in the gut–brain axis are under ongoing [...] Read more.
The role of the intestinal microbiota and its influence on neurodegenerative disorders has recently been extensively explored, especially in the context of Parkinson’s disease (PD). In particular, its role in immunomodulation, impact on inflammation, and participation in the gut–brain axis are under ongoing investigations. Recent studies have revealed new data that could be important for exploring the neurodegeneration mechanisms connected with the gut microbiota, potentially leading to the development of new methods of treatment. In this review, the potential roles of the gut microbiota in future disease-modifying therapies were discussed and the properties of the intestinal microbiota—including its impacts on metabolism and short-chain fatty acids and vitamins—were summarized, with a particular focus on atypical Parkinsonian syndromes. This review focused on a detailed description of the numerous mechanisms through which the microbiota influences neurodegenerative processes. This review explored potentially important connections between the gut microbiota and the evolution and progression of atypical Parkinsonian syndromes. Finally, a description of recently derived results regarding the microbiota alterations in atypical Parkinsonian syndromes in comparison with results previously described in PD was also included. Full article
(This article belongs to the Special Issue Advances in Neurodegenerative Diseases Research and Therapy—Third Edition)
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21 pages, 623 KiB  
Review
A Comprehensive Examination of the Role of Epigenetic Factors in Multiple Sclerosis
by Ida Manna, Selene De Benedittis and Danilo Porro
Int. J. Mol. Sci. 2024, 25(16), 8921; https://doi.org/10.3390/ijms25168921 - 16 Aug 2024
Cited by 3 | Viewed by 2083
Abstract
According to various research, the risk of multiple sclerosis (MS) is strongly influenced by genetic variations. Population, familial, and molecular studies provide strong empirical support for a polygenic pattern of inheritance, mainly due to relatively common allelic variants in the general population. The [...] Read more.
According to various research, the risk of multiple sclerosis (MS) is strongly influenced by genetic variations. Population, familial, and molecular studies provide strong empirical support for a polygenic pattern of inheritance, mainly due to relatively common allelic variants in the general population. The strongest MS susceptibility locus, which was unmistakably identified in tested populations, is the major histocompatibility complex on chromosome 6p21.3. However, the effect of a given predisposing variant remains modest, so there is the possibility that multiple gene–gene and/or gene–environment interactions could significantly increase the contribution of specific variants to the overall genetic risk. Furthermore, as is known, susceptibility genes can be subject to epigenetic modifications, which greatly increase the complexity of MS heritability. Investigating epigenetic and environmental factors can provide new opportunities for the molecular basis of the MS, which shows complicated pathogenesis. Although studies of epigenetic changes in MS only began in the last decade, a growing body of literature suggests that these may be involved in the development of MS. Here, we summarize recent studies regarding epigenetic changes related to MS initiation and progression. Furthermore, we discuss how current studies address important clinical questions and how future studies could be used in clinical practice. Full article
(This article belongs to the Special Issue Advances in Neurodegenerative Diseases Research and Therapy—Third Edition)
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Other

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10 pages, 1521 KiB  
Opinion
The Genetic Background of the Immunological and Inflammatory Aspects of Progressive Supranuclear Palsy
by Piotr Alster and Natalia Madetko-Alster
Int. J. Mol. Sci. 2025, 26(9), 3927; https://doi.org/10.3390/ijms26093927 - 22 Apr 2025
Viewed by 173
Abstract
Progressive supranuclear palsy (PSP) is a neurodegenerative disease, classified as an atypical Parkinsonian syndrome, that has been pathologically and clinically defined. The histopathological aspects of the disease include tufted astrocytes, while the clinical features involve oculomotor dysfunction, postural instability, akinesia, cognitive impairment, and [...] Read more.
Progressive supranuclear palsy (PSP) is a neurodegenerative disease, classified as an atypical Parkinsonian syndrome, that has been pathologically and clinically defined. The histopathological aspects of the disease include tufted astrocytes, while the clinical features involve oculomotor dysfunction, postural instability, akinesia, cognitive impairment, and language difficulties. Although PSP is generally considered a sporadic disease, interest is growing in its genetics, with contemporary research focusing on familial backgrounds and neuroinflammation. Indeed, microglial activation and other inflammatory mechanisms of PSP pathogenesis have been extensively analyzed using genetic examinations to identify the factors impacting neurodegeneration. As such, this review aims to elaborate on recent findings in this field. Full article
(This article belongs to the Special Issue Advances in Neurodegenerative Diseases Research and Therapy—Third Edition)
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