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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 March 2025 | Viewed by 2426

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.

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

  • neurodegenerative diseases
  • therapy
  • molecular mechanisms
  • neuron
  • astrocytes
  • microglia
  • inflammation
  • brain
  • drug delivery

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Published Papers (2 papers)

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Research

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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 1004
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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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
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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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