Special Issue "Cellular and Molecular Mechanisms of Neurodegenerative Diseases"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 20 January 2022.

Special Issue Editor

Prof. Adrian Israelson
E-Mail Website
Guest Editor
Ben-Gurion University of the Negev, Beer Sheba, Israel
Interests: ALS; neurodegeneration; misfolded proteins; misfolded SOD1; mutant SOD1 models; protein aggregation; MIF; chaperones; mitochondrial dysfunction

Special Issue Information

Dear colleagues,

Neurodegenerative diseases (Alzheimer’s disease, Parkinson’s disease, ALS, etc.) currently represent a major challenge to public health worldwide, especially as our population continues to age. Neurodegeneration is characterized by the progressive degeneration of specific neuronal populations driven by, as of yet, unknown cellular and molecular pathogenic mechanisms. Since there is no cure or effective treatment for these disorders, the characterization of the specific mechanisms that lead to neurodegeneration, as well as the identification of potential novel targets for the development of new therapeutic strategies, is a major priority in this field.

The aim of this Special Issue is to provide an overview of the main cellular and molecular pathogenic mechanisms, elucidated thus far, that lead to the onset and progression of these devastating neurodegenerative disorders, highlighting both the common and specific pathways involved in each one of them.

Prof. Adrian Israelson
Guest Editor

Manuscript Submission Information

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Keywords

  • neurodegeneration
  • Alzheimer’s disease
  • Parkinson’s disease
  • Huntington’s disease
  • motor neuron disease
  • amyotrophic lateral sclerosis
  • ALS
  • neurodegenerative diseases
  • ER stress
  • mitochondrial dysfunction
  • misfolded proteins
  • protein aggregation

Published Papers (3 papers)

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Review

Review
All Roads Lead to Rome: Different Molecular Players Converge to Common Toxic Pathways in Neurodegeneration
Cells 2021, 10(9), 2438; https://doi.org/10.3390/cells10092438 - 16 Sep 2021
Cited by 1 | Viewed by 991
Abstract
Multiple neurodegenerative diseases (NDDs) such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD) are being suggested to have common cellular and molecular pathological mechanisms, characterized mainly by protein misfolding and aggregation. These large inclusions, most likely, [...] Read more.
Multiple neurodegenerative diseases (NDDs) such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD) are being suggested to have common cellular and molecular pathological mechanisms, characterized mainly by protein misfolding and aggregation. These large inclusions, most likely, represent an end stage of a molecular cascade; however, the soluble misfolded proteins, which take part in earlier steps of this cascade, are the more toxic players. These pathological proteins, which characterize each specific disease, lead to the selective vulnerability of different neurons, likely resulting from a combination of different intracellular mechanisms, including mitochondrial dysfunction, ER stress, proteasome inhibition, excitotoxicity, oxidative damage, defects in nucleocytoplasmic transport, defective axonal transport and neuroinflammation. Damage within these neurons is enhanced by damage from the nonneuronal cells, via inflammatory processes that accelerate the progression of these diseases. In this review, while acknowledging the hallmark proteins which characterize the most common NDDs; we place specific focus on the common overlapping mechanisms leading to disease pathology despite these different molecular players and discuss how this convergence may occur, with the ultimate hope that therapies effective in one disease may successfully translate to another. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Neurodegenerative Diseases)
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Review
Intersection of Redox Chemistry and Ubiquitylation: Post-Translational Modifications Required for Maintaining Cellular Homeostasis and Neuroprotection
Cells 2021, 10(8), 2121; https://doi.org/10.3390/cells10082121 - 18 Aug 2021
Viewed by 419
Abstract
Neurodegeneration has been predominantly recognized as neuronal breakdown induced by the accumulation of aggregated and/or misfolded proteins and remains a preliminary factor in age-dependent disease. Recently, critical regulating molecular mechanisms and cellular pathways have been shown to induce neurodegeneration long before aggregate accumulation [...] Read more.
Neurodegeneration has been predominantly recognized as neuronal breakdown induced by the accumulation of aggregated and/or misfolded proteins and remains a preliminary factor in age-dependent disease. Recently, critical regulating molecular mechanisms and cellular pathways have been shown to induce neurodegeneration long before aggregate accumulation could occur. Although this opens the possibility of identifying biomarkers for early onset diagnosis, many of these pathways vary in their modes of dysfunction while presenting similar clinical phenotypes. With selectivity remaining difficult, it is promising that these neuroprotective pathways are regulated through the ubiquitin-proteasome system (UPS). This essential post-translational modification (PTM) involves the specific attachment of ubiquitin onto a substrate, specifically marking the ubiquitin-tagged protein for its intracellular fate based upon the site of attachment, the ubiquitin chain type built, and isopeptide linkages between different ubiquitin moieties. This review highlights both the direct and indirect impact ubiquitylation has in oxidative stress response and neuroprotection, and how irregularities in these intricate processes lead towards the onset of neurodegenerative disease (NDD). Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Neurodegenerative Diseases)
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Review
Role of Kynurenine Pathway in Oxidative Stress during Neurodegenerative Disorders
Cells 2021, 10(7), 1603; https://doi.org/10.3390/cells10071603 - 26 Jun 2021
Cited by 1 | Viewed by 779
Abstract
Neurodegenerative disorders are chronic and life-threatening conditions negatively affecting the quality of patients’ lives. They often have a genetic background, but oxidative stress and mitochondrial damage seem to be at least partly responsible for their development. Recent reports indicate that the activation of [...] Read more.
Neurodegenerative disorders are chronic and life-threatening conditions negatively affecting the quality of patients’ lives. They often have a genetic background, but oxidative stress and mitochondrial damage seem to be at least partly responsible for their development. Recent reports indicate that the activation of the kynurenine pathway (KP), caused by an activation of proinflammatory factors accompanying neurodegenerative processes, leads to the accumulation of its neuroactive and pro-oxidative metabolites. This leads to an increase in the oxidative stress level, which increases mitochondrial damage, and disrupts the cellular energy metabolism. This significantly reduces viability and impairs the proper functioning of central nervous system cells and may aggravate symptoms of many psychiatric and neurodegenerative disorders. This suggests that the modulation of KP activity could be effective in alleviating these symptoms. Numerous reports indicate that tryptophan supplementation, inhibition of KP enzymes, and administration or analogs of KP metabolites show promising results in the management of neurodegenerative disorders in animal models. This review gathers and systematizes the knowledge concerning the role of metabolites and enzymes of the KP in the development of oxidative damage within brain cells during neurodegenerative disorders and potential strategies that could reduce the severity of this process. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Neurodegenerative Diseases)
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