Protein Misfolding Diseases: From Experimental Approaches to Therapeutic Opportunities

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

Deadline for manuscript submissions: 25 February 2025 | Viewed by 4229

Special Issue Editors

Premedical Division, Weill Cornell Medicine-Qatar, Education City, Qatar
Interests: amyloid protein; neurodegenerative diseases; type 2 diabetes; biophysics

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Guest Editor
Department of Experimental Neurodegeneration, University Medical Center Göttingen, Göttingen, Germany
Interests: neurodegeneration; Parkinson’s disease; Alzheimer’s disease; protein aggregation
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Special Issue Information

Dear Colleagues,

Protein misfolding and amyloid formation are the pathognomonic modalities behind the most globally prevalent neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease. With the worldwide prevalence of dementia, a common pathological consequence of these neurodegenerative diseases that is expected to almost triple in less than thirty years, they pose significant challenges to healthcare systems worldwide. Strikingly, protein aggregation seems to also be an important hallmark in other highly prevalent diseases, such as cancer and diabetes, suggesting that shared mechanisms may be involved.

This Special Issue welcomes review articles and original reports that will improve our understanding of the mechanisms involved in protein misfolding diseases. A deeper understanding of these mechanisms, and the cross-fertilization between different fields will create opportunities for developing novel diagnostics and treatment modalities for many devastating diseases.

Dr. Ali Chaari
Prof. Dr. Tiago Fleming Outeiro
Guest Editors

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Keywords

  • protein aggregation
  • amyloid
  • neurodegenerative diseases
  • cancer
  • diabetes

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Published Papers (2 papers)

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Research

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14 pages, 1823 KiB  
Article
The Protein Network in Subcutaneous Fat Biopsies from Patients with AL Amyloidosis: More Than Diagnosis?
by Dario Di Silvestre, Francesca Brambilla, Francesca Lavatelli, Maila Chirivì, Diana Canetti, Claudia Bearzi, Roberto Rizzi, Johan Bijzet, Bouke P. C. Hazenberg, Vittorio Bellotti, Julian D. Gillmore and Pierluigi Mauri
Cells 2023, 12(5), 699; https://doi.org/10.3390/cells12050699 - 22 Feb 2023
Cited by 2 | Viewed by 2016
Abstract
AL amyloidosis is caused by the misfolding of immunoglobulin light chains leading to an impaired function of tissues and organs in which they accumulate. Due to the paucity of -omics profiles from undissected samples, few studies have addressed amyloid-related damage system wide. To [...] Read more.
AL amyloidosis is caused by the misfolding of immunoglobulin light chains leading to an impaired function of tissues and organs in which they accumulate. Due to the paucity of -omics profiles from undissected samples, few studies have addressed amyloid-related damage system wide. To fill this gap, we evaluated proteome changes in the abdominal subcutaneous adipose tissue of patients affected by the AL isotypes κ and λ. Through our retrospective analysis based on graph theory, we have herein deduced new insights representing a step forward from the pioneering proteomic investigations previously published by our group. ECM/cytoskeleton, oxidative stress and proteostasis were confirmed as leading processes. In this scenario, some proteins, including glutathione peroxidase 1 (GPX1), tubulins and the TRiC complex, were classified as biologically and topologically relevant. These and other results overlap with those already reported for other amyloidoses, supporting the hypothesis that amyloidogenic proteins could induce similar mechanisms independently of the main fibril precursor and of the target tissues/organs. Of course, further studies based on larger patient cohorts and different tissues/organs will be essential, which would be a key point that would allow for a more robust selection of the main molecular players and a more accurate correlation with clinical aspects. Full article
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Review

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15 pages, 1096 KiB  
Review
Immunotherapy for Parkinson’s Disease and Alzheimer’s Disease: A Promising Disease-Modifying Therapy
by Anns Mahboob, Hasan Ali, AlJazi AlNaimi, Mahmoud Yousef, Mlaak Rob, Nawaf Ahmad Al-Muhannadi, Degiri Kalana Lasanga Senevirathne and Ali Chaari
Cells 2024, 13(18), 1527; https://doi.org/10.3390/cells13181527 - 12 Sep 2024
Cited by 1 | Viewed by 1290
Abstract
Alzheimer’s disease (AD) and Parkinson’s disease (PD) are two neurodegenerative diseases posing a significant disease burden due to their increasing prevalence and socio-economic cost. Traditional therapeutic approaches for these diseases exist but provide limited symptomatic relief without addressing the underlying pathologies. This review [...] Read more.
Alzheimer’s disease (AD) and Parkinson’s disease (PD) are two neurodegenerative diseases posing a significant disease burden due to their increasing prevalence and socio-economic cost. Traditional therapeutic approaches for these diseases exist but provide limited symptomatic relief without addressing the underlying pathologies. This review examines the potential of immunotherapy, specifically monoclonal antibodies (mAbs), as disease-modifying treatments for AD and PD. We analyze the pathological mechanisms of AD and PD, focusing on the roles of amyloid-beta (Aβ), tau (τ), and alpha-synuclein (α-syn) proteins. We discuss the latest advancements in mAb therapies targeting these proteins, evaluating their efficacy in clinical trials and preclinical studies. We also explore the challenges faced in translating these therapies from bench to bedside, including issues related to safety, specificity, and clinical trial design. Additionally, we highlight future directions for research, emphasizing the need for combination therapies, improved biomarkers, and personalized treatment strategies. This review aims to provide insights into the current state and future potential of antibody-based immunotherapy in modifying the course of AD and PD, ultimately improving patient outcomes and quality of life. Full article
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