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Biomedicines
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Advanced Research in Proteinopathies
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Advanced Research in Proteinopathies

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 3601

Special Issue Editors

Dr. Claudia Capitini

E-Mail Website
Guest Editor
LENS-European Laboratory for Non-Linear Spectroscopy, Sesto Fiorentino, Italy
Interests: neurodegeneration; drug investigation; protein aggregation; translational research
Special Issues, Collections and Topics in MDPI journals
Dr. Manuela Leri

E-Mail Website
Guest Editor
Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Viale Morgagni 50, 50134 Florence, Italy
Interests: amyloid aggregation; autophagy; natural polyphenols; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Proteinopathies are a family of diseases characterized by the accumulation of specific proteins within neurons or in the brain parenchyma that lead to synaptic dysfunction and neuronal loss. Examples for proteinopathies are Alzheimer’s disease, Parkinson’s disease, Lewy body disease, amyotrophic lateral sclerosis and fronto-temporal lobar degeneration. Typically, in a disease condition, the unstructured proteins change their conformation leading to small oligomers that eventually aggregate into higher-order structures. Prion disease is an exception within the family of proteinopathies, as the aggregated prion protein is highly infectious and can self-aggregate and propagate.

Over the years, the structural and morphological features of several protein aggregate species have been investigated, as well as the cellular events that lead to neuronal dysfunction. Moreover, a number of potential therapeutic strategies have been explored, including small molecules, antibodies and natural compounds, some of them showing promising outcomes.

This Special Issue welcomes the submission of original research papers and reviews on the most advanced developments in the above-mentioned topics, with special attention on possible therapeutic approaches targeting misfolded proteins.

Dr. Claudia Capitini
Dr. Manuela Leri
Guest Editors

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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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 misfolding
  • oligomers
  • amyloid fibrils
  • amorphous aggregates
  • prion
  • neurodegeneration
  • aggregation kinetics
  • neurotoxicity
  • drug discovery

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Published Papers (2 papers)

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Research

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16 pages, 1778 KiB  
Article
SIMOA Diagnostics on Alzheimer’s Disease and Frontotemporal Dementia
by Athanasia Chatziefstathiou, Sezgi Canaslan, Eirini Kanata, Kostas Vekrellis, Vasilios C. Constantinides, George P. Paraskevas, Elisabeth Kapaki, Matthias Schmitz, Inga Zerr, Konstantinos Xanthopoulos, Theodoros Sklaviadis and Dimitra Dafou
Biomedicines 2024, 12(6), 1253; https://doi.org/10.3390/biomedicines12061253 - 4 Jun 2024
Cited by 2 | Viewed by 2189
Abstract
Background: Accurate diagnosis of Alzheimer’s disease (AD) and frontotemporal dementia (FTD) represents a health issue due to the absence of disease traits. We assessed the performance of a SIMOA panel in cerebrospinal fluid (CSF) from 43 AD and 33 FTD patients with 60 [...] Read more.
Background: Accurate diagnosis of Alzheimer’s disease (AD) and frontotemporal dementia (FTD) represents a health issue due to the absence of disease traits. We assessed the performance of a SIMOA panel in cerebrospinal fluid (CSF) from 43 AD and 33 FTD patients with 60 matching Control subjects in combination with demographic–clinical characteristics. Methods: 136 subjects (AD: n = 43, FTD: n = 33, Controls: n = 60) participated. Single-molecule array (SIMOA), glial fibrillary acidic protein (GFAP), neurofilament light (NfL), TAU, and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) in CSF were analyzed with a multiplex neuro 4plex kit. Receiver operating characteristic (ROC) curve analysis compared area under the curve (AUC), while the principal of the sparse partial least squares discriminant analysis (sPLS-DA) was used with the intent to strengthen the identification of confident disease clusters. Results: CSF exhibited increased levels of all SIMOA biomarkers in AD compared to Controls (AUCs: 0.71, 0.86, 0.92, and 0.94, respectively). Similar patterns were observed in FTD with NfL, TAU, and UCH-L1 (AUCs: 0.85, 0.72, and 0.91). sPLS-DA revealed two components explaining 19% and 9% of dataset variation. Conclusions: CSF data provide high diagnostic accuracy among AD, FTD, and Control discrimination. Subgroups of demographic–clinical characteristics and biomarker concentration highlighted the potential of combining different kinds of data for successful and more efficient cohort clustering. Full article
(This article belongs to the Special Issue Advanced Research in Proteinopathies)
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Review

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21 pages, 315 KiB  
Review
Unraveling the Role of Proteinopathies in Parasitic Infections
by Mikołaj Hurła, Damian Pikor, Natalia Banaszek-Hurła, Alicja Drelichowska, Jolanta Dorszewska, Wojciech Kozubski, Elżbieta Kacprzak and Małgorzata Paul
Biomedicines 2025, 13(3), 610; https://doi.org/10.3390/biomedicines13030610 - 3 Mar 2025
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Abstract
Proteinopathies, characterized by the misfolding, aggregation, and deposition of proteins, are hallmarks of various neurodegenerative and systemic diseases. Increasingly, research has highlighted the role of protein misfolding in parasitic infections, unveiling intricate interactions between host and parasite that exacerbate disease pathology and contribute [...] Read more.
Proteinopathies, characterized by the misfolding, aggregation, and deposition of proteins, are hallmarks of various neurodegenerative and systemic diseases. Increasingly, research has highlighted the role of protein misfolding in parasitic infections, unveiling intricate interactions between host and parasite that exacerbate disease pathology and contribute to chronic outcomes. The life cycles of parasitic protozoa, including Plasmodium, Toxoplasmosis, and Leishmania species, are complicated and involve frequent changes between host and vector environments. Their proteomes are severely stressed during these transitions, which calls for highly specialized protein quality control systems. In order to survive harsh intracellular conditions during infection, these parasites have been demonstrated to display unique adaptations in the unfolded protein response, a crucial pathway controlling endoplasmic reticulum stress. In addition to improving parasite survival, these adaptations affect host cell signaling and metabolism, which may jeopardize cellular homeostasis. By causing oxidative stress, persistent inflammation, and disturbance of cellular proteostasis, host–parasite interactions also contribute to proteinopathy. For instance, Plasmodium falciparum disrupts normal protein homeostasis and encourages the accumulation of misfolded proteins by influencing host redox systems involved in protein folding. In addition to interfering with host chaperone systems, the parasitic secretion of effector proteins exacerbates protein misfolding and aggregate formation. Autophagy, apoptosis regulation, organelle integrity, and other vital cellular processes are all disrupted by these pathological protein aggregates. Long-term misfolding and aggregation can cause irreversible tissue damage, which can worsen the clinical course of illnesses like visceral leishmaniasis, cerebral malaria, and toxoplasmosis. Treating parasite-induced proteinopathies is a potentially fruitful area of therapy. According to recent research, autophagy modulators, proteasome enhancers, and small-molecule chaperones may be repurposed to lessen these effects. Pharmacological agents that target the UPR, for example, have demonstrated the ability to decrease parasite survival while also reestablishing host protein homeostasis. Targeting the proteins secreted by parasites that disrupt host proteostasis may also offer a novel way to stop tissue damage caused by proteinopathies. In conclusion, the intersection of protein misfolding and parasitic infections represents a rapidly advancing field of research. Dissecting the molecular pathways underpinning these processes offers unprecedented opportunities for developing innovative therapies. These insights could not only transform the management of parasitic diseases but also contribute to a broader understanding of proteinopathies in infectious and non-infectious diseases alike. Full article
(This article belongs to the Special Issue Advanced Research in Proteinopathies)
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