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: closed (31 July 2024) | Viewed by 3422

Special Issue Editor


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

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

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

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

16 pages, 1670 KiB  
Review
Glymphatic System Pathology and Neuroinflammation as Two Risk Factors of Neurodegeneration
by Stanisław Szlufik, Kamila Kopeć, Stanisław Szleszkowski and Dariusz Koziorowski
Cells 2024, 13(3), 286; https://doi.org/10.3390/cells13030286 - 5 Feb 2024
Cited by 2 | Viewed by 3020
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
Show Figures

Figure 1

Back to TopTop