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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 3457

Special Issue Editor


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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
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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

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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 (3 papers)

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Research

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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
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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
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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
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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
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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
Viewed by 1105
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
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