Cellular Regulation of Pathological Proteins in Neurodegenerative Disease

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

Deadline for manuscript submissions: 31 July 2024 | Viewed by 977

Special Issue Editor

Dr. Sonia Sirisi
E-Mail Website
Guest Editor
Institut d’Investigació Biomèdica Sant Pau (IIB), Sant Quintí 77-79, 08041 Barcelona, Spain
Interests: neuropathology; Alzheimer’s disease; APP; tau; toxic mechanisms; processing pathways

Special Issue Information

Dear Colleagues,

In some neurodegenerative diseases, the pathology is characterised by the presence of toxic proteins that accumulate in aggregates in the brain. The aggregates and/or oligomers appear to be toxic, causing injury or cell death. However, the role of these aggregates in disease is not fully understood. These pathological proteins are implicated in neurodegenerative diseases that trigger progressive degeneration through largely unknown pathogenic mechanisms, and lack valid therapeutic approaches. In this Special Issue, the focus will be on the cellular regulation of pathological proteins in neurodegenerative diseases such as Alzheimer's disease (AD), Huntington’s disease (HD), Parkinson's disease (PD), frontotemporal dementia (FTD), dementia with Lewy bodies (DLB), amyotrophic lateral sclerosis (ALS) and prion disease (PrD).

This Special Issue will highlight the current knowledge on the regulation of pathological aggregates that form in neurodegenerative diseases.

Dr. Sonia Sirisi
Guest Editor

Manuscript Submission Information

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Keywords

  • protein aggregates
  • neurodegeneration
  • neurodegenerative diseases
  • regulation pathways
  • misfolded proteins
  • toxic proteins
  • homeostasis
  • autophagy

Published Papers (1 paper)

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Review

16 pages, 1670 KiB  
Review
Glymphatic System Pathology and Neuroinflammation as Two Risk Factors of Neurodegeneration
Cells 2024, 13(3), 286; https://doi.org/10.3390/cells13030286 - 05 Feb 2024
Viewed by 754
Abstract
The key to the effective treatment of neurodegenerative disorders is a thorough understanding of their pathomechanism. Neurodegeneration and neuroinflammation are mutually propelling brain processes. An impairment of glymphatic system function in neurodegeneration contributes to the progression of pathological processes. The question arises as [...] Read more.
The key to the effective treatment of neurodegenerative disorders is a thorough understanding of their pathomechanism. Neurodegeneration and neuroinflammation are mutually propelling brain processes. An impairment of glymphatic system function in neurodegeneration contributes to the progression of pathological processes. The question arises as to how neuroinflammation and the glymphatic system are related. This review highlights the direct and indirect influence of these two seemingly independent processes. Protein aggregates, a characteristic feature of neurodegeneration, are correlated with glymphatic clearance and neuroinflammation. Glial cells cannot be overlooked when considering the neuroinflammatory processes. Astrocytes are essential for the effective functioning of the glymphatic system and play a crucial role in the inflammatory responses in the central nervous system. It is imperative to acknowledge the significance of AQP4, a protein that exhibits a high degree of polarization in astrocytes and is crucial for the functioning of the glymphatic system. AQP4 influences inflammatory processes that have not yet been clearly delineated. Another interesting issue is the gut–brain axis and microbiome, which potentially impact the discussed processes. A discussion of the correlation between the functioning of the glymphatic system and neuroinflammation may contribute to exploring the pathomechanism of neurodegeneration. Full article
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Glymphatic system pathology and neuroinflammation as two risk factors of neurodegeneration
Authors: Stanisław Szlufik; Kamila Kopeć; Stanisław Szleszkowski; Dariusz Koziorowski
Affiliation: Department of Neurology, Faculty of Health Science, Medical University of Warsaw
Abstract: Neurodegenerative disorders are among the main challenges in modern neurology. The key to the effective treatment of the disease is a thorough understanding of its pathomechanism. The role of neuroinflammation in the pathogenesis of neurodegenerative disorders has been emphasized for many years. Neurodegeneration and neuroinflammation are mutually propelling processes in the brain. However, the glymphatic system appears to play a significant role in this cycle. Impairment of glymphatic system function in neurodegeneration contributes to the progression of pathological processes. The question arises about how neuroinflammation and the glymphatic system are related, and whether it is possible to determine how they affect each other. This review highlights the direct and indirect influence of these two seemingly independent processes. Protein aggregates, a characteristic feature of neurodegeneration, correlate with glymphatic clearance and neuroinflammation. Glial cells cannot be overlooked when considering the neuroinflammatory processes. Astrocytes perform a broad range of functions. These cells are essential for the effective functioning of the glymphatic system and play a crucial role in the inflammatory responses in the central nervous system. Another interesting issue is the gut-brain axis and microbiome, which potentially impact the discussed processes. The complexity of the problem makes it impossible to provide unambiguous answers to the questions posed. However, starting a discussion on the correlation between the functioning of the glymphatic system and neuroinflammation may contribute to exploring the pathomechanism of neurodegeneration

Title: Transcriptome wide correlations with neuropathological hallmarks in the frontal cortex of FTLD-TDP patients
Authors: Oriol Dols-Icardo, Sònia Sirisi Dolcet, Natalia Valle Tamayo, Victor Montal, Érika Sánchez-Aced, Laura Molina, Ignacio Illán-Gala, Jordi Pegueroles, Alba Cervantes-González, Olivia Belbin, Juan Fortea
Affiliation: Memory Unit. Neurology Department and Sant Pau Biomedical Research Institute, Hospital de la Santa Creu i Sant Pau, Universitat Autonoma de Barcelona; Network Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED)

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