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Special Issue "Molecular Mechanisms of Aging-Related Neurodegenerative Diseases"

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: 30 June 2021.

Special Issue Editor

Prof. Dr. Urszula Wojda
E-Mail Website
Guest Editor
Laboratory of Preclinical Testing of Higher Standard, Neurobiology Center, Nencki Institute of Experimental Biology, 3 Pasteur Str., 02-093 Warsaw, Poland
Interests: Alzheimer’s disease; molecular mechanisms of neurodegeneration; diagnostics; prognostics; biomarkers; machine learning; artificial intelligence

Special Issue Information

Dear Colleague,

Aging is the main risk factor for many neurodegenerative diseases, including the most common: Alzheimer’s disease and Parkinson’s disease. These diseases are sporadic in the majority of cases, irreversibly escalate with time, and eventually lead to massive neuronal loss. They represent a large, global socioeconomic burden, with no effective therapies available.

Brain cells are especially sensitive to the aging process, but the pathomechanisms switching non-pathological aging to neurodegenerative disorders are complex and not yet fully elucidated. It seems that neurodegeneration develops gradually as a crosstalk between systemic metabolic and inflammatory changes and the brain and involves impairment in the blood–brain barrier and neuroinflammation. Many genetic, epigenetic, and environmental factors, including infectious agents, can contribute to neurodegeneration. Molecular mechanisms of the pathogenesis comprise, but are not limited to, loss of proteostasis, mitochondrial impairment, oxidative stress, cell cycle dysregulation, genomic instability, and calcium dyshomeostasis. 

As the elucidation of molecular mechanisms and the sequence of pathological events driving neurodegenerative diseases is crucial for the development of efficient therapies, this Special Issue invites submissions of original research articles and short or comprehensive reviews presenting the current developments in this area. Articles with a therapeutic perspective are especially welcome.

Prof. Dr. Urszula Wojda
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 papers will be 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

  • Aging
  • Neurodegenerative diseases
  • Alzheimer’s disease
  • Parkinson’s disease
  • Neuroinflammation
  • Oxidative stress
  • Mitochondrial disorder
  • Calcium dyshomeostasis
  • Genomic instability
  • Epigenetic dysregulation
  • Novel therapeutic target

Published Papers (1 paper)

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Research

Open AccessArticle
The ALS-Associated FUS (P525L) Variant Does Not Directly Interfere with Microtubule-Dependent Kinesin-1 Motility
Int. J. Mol. Sci. 2021, 22(5), 2422; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052422 - 28 Feb 2021
Viewed by 534
Abstract
Deficient intracellular transport is a common pathological hallmark of many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Mutations in the fused-in-sarcoma (FUS) gene are one of the most common genetic causes for familial ALS. Motor neurons carrying a mutation in the nuclear localization [...] Read more.
Deficient intracellular transport is a common pathological hallmark of many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Mutations in the fused-in-sarcoma (FUS) gene are one of the most common genetic causes for familial ALS. Motor neurons carrying a mutation in the nuclear localization sequence of FUS (P525L) show impaired axonal transport of several organelles, suggesting that mislocalized cytoplasmic FUS might directly interfere with the transport machinery. To test this hypothesis, we studied the effect of FUS on kinesin-1 motility in vitro. Using a modified microtubule gliding motility assay on surfaces coated with kinesin-1 motor proteins, we showed that neither recombinant wildtype and P525L FUS variants nor lysates from isogenic ALS-patient-specific iPSC-derived spinal motor neurons expressing those FUS variants significantly affected gliding velocities. We hence conclude that during ALS pathogenesis the initial negative effect of FUS (P525L) on axonal transport is an indirect nature and requires additional factors or mechanisms. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Aging-Related Neurodegenerative Diseases)
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