Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.2
4.8
Journals
Biomolecules
Special Issues
Biomarkers in Neurodegenerative Diseases: Shaping the Future of Diagnosis and...
share announcement

Biomarkers in Neurodegenerative Diseases: Shaping the Future of Diagnosis and Treatment

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biomarkers".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 1292

Special Issue Editors

Dr. Martine Tétreault

E-Mail Website1 Website2
Guest Editor
Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada
Interests: neuromuscular and neurodegenerative diseases; genetics; molecular biology
Dr. Laura Hamilton

E-Mail Website1 Website2
Co-Guest Editor
Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, QC, Canada
Interests: lipids; omics; neurodegenerative diseases

Special Issue Information

Dear Colleagues,

We invite researchers and experts to contribute articles focused on the transformative role of biomarkers in neurodegenerative disorders. As we stand at the threshold of new breakthroughs in understanding diseases like Alzheimer's, Parkinson’s, and other neurodegenerative conditions, biomarkers are becoming essential for shaping the future of diagnosis, treatment, and patient care. We welcome submissions that explore the latest innovations, cutting-edge research, and the critical impact that biomarkers have on early detection, disease progression, and personalized therapeutic approaches. Join us in advancing the science that will revolutionize the management and treatment of neurodegenerative diseases.

Dr. Martine Tétreault
Dr. Laura Hamilton
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. Biomolecules 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 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

  • molecular diagnostics
  • lipidomics
  • genomics
  • proteomics
  • transcriptomics

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.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

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

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

17 pages, 2167 KB  
Article
Expression of Reelin, Aβ1-42, Tau and FTH1 in Idiopathic Epiretinal Membranes: Exploring the Link Between Reelin and Neurodegenerative Biomarkers
by Bijorn Omar Balzamino, Graziana Esposito, Pamela Cosimi, Rosanna Squitti, Giuseppina Amadoro, Valentina Latina, Guido Ripandelli, Andrea Cacciamani and Alessandra Micera
Biomolecules 2025, 15(8), 1187; https://doi.org/10.3390/biom15081187 - 18 Aug 2025
Viewed by 430
Abstract
Growing evidence suggests that Reelin signals and cleavages are affected in neurodegenerative diseases, prospecting a potential role for Reelin in the pathogenesis of neurodegenerative processes occurring in insulted retinas. We sought to determine whether Reelin, Aβ1-42, FTH1 and TAU proteins accumulate in ocular [...] Read more.
Growing evidence suggests that Reelin signals and cleavages are affected in neurodegenerative diseases, prospecting a potential role for Reelin in the pathogenesis of neurodegenerative processes occurring in insulted retinas. We sought to determine whether Reelin, Aβ1-42, FTH1 and TAU proteins accumulate in ocular fluids of idiopathic epiretinal membrane (iERM) specimens and whether such accumulations depend on disease severity. Comparisons and correlation studies were used to verify the hypothesis of a Reelin, Aβ1-42, TAU and FTH1 marker expressions in this vitreoretinal disease, extending the knowledge on the pathological spectrum of neurodegenerative eye diseases. Aqueous, vitreous and peeled-off ERM samples were collected from patients who had undergone vitrectomy and grouped according to disease severity. We found out that Reelin and Aβ1-42 were expressed in ocular fluids and affected ERMs depending on disease severity. At stage 3, higher Reelin and Aβ1-42 immunofluorescence staining was detected in ERMs, in agreement with the higher Reelin, Aβ1-42, FTH1 and TAU transcript expressions by RT-PCR. Differential expressions of transcripts specific to Aβ1-42, FTH1, GFAP and TAU occurred in vitreal hyalocytes and astrocytes, which selectively responded to vitreal exposure. This is the first study reporting the association between Reelin and ERM disease, highlighting the potential role of Reelin in neurodegenerating and Drusen-affected retinas. The potential association of neurodegenerative mediators with ERM would suggest that part of the neuronal damage activated at the vitreoretinal interphase might be driven by Reelin. Full article
(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases: Shaping the Future of Diagnosis and Treatment)
►▼ Show Figures

Figure 1

Review

Jump to: Research

21 pages, 1238 KB  
Review
Complement Cascades and Brain Disorders
by Ivana Jovčevska, Alja Videtič Paska and Katarina Kouter
Biomolecules 2025, 15(8), 1179; https://doi.org/10.3390/biom15081179 - 17 Aug 2025
Viewed by 589
Abstract
The complement system is a vital component of innate immunity. Besides its roles in pathogen defense, its significance in neurodevelopment, neurodegeneration, and cancer progression is beginning to be recognized. We performed a comprehensive literature review to summarize the involvement and dysregulation of the [...] Read more.
The complement system is a vital component of innate immunity. Besides its roles in pathogen defense, its significance in neurodevelopment, neurodegeneration, and cancer progression is beginning to be recognized. We performed a comprehensive literature review to summarize the involvement and dysregulation of the complement system in three main CNS-associated conditions: Alzheimer’s disease, schizophrenia, and glioma. In Alzheimer’s disease, activation of the complement system contributes to neuroinflammation, synaptic loss, and neuronal death. In glioblastoma, complement promotes tumor growth, immune evasion, and therapy resistance. In schizophrenia, genetic variations in complement components, particularly C4A, are associated with synaptic pruning abnormalities and disease susceptibility. We conclude that the complement system has a dual role of protector and pathogenic mediator in the central nervous system. While it is critical in neurodegenerative, oncological, and psychiatric disorders, its role is not understood well enough. For therapeutic purposes, targeting the complement system may open new frontiers for therapeutic interventions without disrupting important physiological processes. More research is needed to elucidate the exact roles of the complement and help translate these findings into clinical settings. Full article
(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases: Shaping the Future of Diagnosis and Treatment)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop