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Biomolecules
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Biomarkers in Neurodegenerative Diseases: Shaping the Future of Diagnosis and...
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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: 30 April 2026 | Viewed by 5353

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, QC, 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 250 words) can be sent to the Editorial Office for assessment.

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

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Published Papers (5 papers)

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Research

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17 pages, 722 KB  
Article
Association of Plasma Placental Growth Factor with White Matter Hyperintensities in Alzheimer’s Disease
by Kazuya Igarashi, Tamao Tsukie, Kazuo Washiyama, Kiyoshi Onda, Yuki Miyagi, Shoya Inagawa, Soichiro Shimizu, Akinori Miyashita, Osamu Onodera, Takeshi Ikeuchi and Kensaku Kasuga
Biomolecules 2025, 15(10), 1367; https://doi.org/10.3390/biom15101367 - 26 Sep 2025
Viewed by 747
Abstract
Autopsy studies have shown that Alzheimer’s disease (AD) often coexists with cerebrovascular injury, affecting cognitive outcomes and the effectiveness of anti-amyloid-beta (Aβ) drugs. No fluid biomarkers of cerebrovascular injury have been identified yet. We investigated the association between white matter hyperintensities (WMH) severity [...] Read more.
Autopsy studies have shown that Alzheimer’s disease (AD) often coexists with cerebrovascular injury, affecting cognitive outcomes and the effectiveness of anti-amyloid-beta (Aβ) drugs. No fluid biomarkers of cerebrovascular injury have been identified yet. We investigated the association between white matter hyperintensities (WMH) severity and fluid biomarkers, including cerebrospinal fluid (CSF) neurofilament light chain and plasma placental growth factor (PlGF) levels. This study included 242 patients from memory clinics. Magnetic resonance imaging (MRI), CSF, and plasma samples were collected. Patients were classified as AD+ or non-AD based on the CSF Aβ42/Aβ40 ratio. In the discovery cohort (79 AD+ and 20 non-AD patients with 3D-T1 images), we analyzed the association between WMH volume and plasma PlGF. In the validation cohort (54 AD+ patients without 3D-T1 images), we analyzed the association between WMH grading and plasma PlGF. Among AD+ patients in the discovery cohort, plasma PlGF levels remained significantly associated with WMH volume and grading after adjusting for age, sex, and global cognition. Among the AD+ patients in the validation cohort, the high-PlGF (above median) group had significantly greater WMH volumes and a higher number of patients with a high WMH grading than the low-PlGF (below median) group. Plasma PlGF is a promising marker of cerebrovascular injury in AD. Full article
(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases: Shaping the Future of Diagnosis and Treatment)
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21 pages, 4606 KB  
Article
Targeting a Tau Kinase Cdk5, Cyclin-Dependent Kinase: A Blood-Based Diagnostic Marker and Therapeutic Earmark for Alzheimer’s Disease
by Sakshi Kumari, Abhinay Kumar Singh, Mukesh Kumar, Rashmita Pradhan, Abhijith R. Rao, Yudhishthir Yadav, Pramod Kumar, Partha Haldar, Punit Kaur and Sharmistha Dey
Biomolecules 2025, 15(10), 1365; https://doi.org/10.3390/biom15101365 - 26 Sep 2025
Viewed by 834
Abstract
Protein kinases are important molecules of Alzheimer’s Disease (AD), driving neuronal demise and the emergence of the disease’s destructive hallmarks. Cdk5 has recently been highlighted as a key therapeutic target for AD. This study evaluated the expression levels of Cdk5 and Mcl1 (Cdk5’s [...] Read more.
Protein kinases are important molecules of Alzheimer’s Disease (AD), driving neuronal demise and the emergence of the disease’s destructive hallmarks. Cdk5 has recently been highlighted as a key therapeutic target for AD. This study evaluated the expression levels of Cdk5 and Mcl1 (Cdk5’s substrate) in blood samples of 61 AD, 55 Mild Cognitive Impairment (MCI), and 57 Geriatric Controls (GC), and explored the in vitro inhibition of Cdk5. The serum levels of Cdk5 and Mcl1 were measured by Surface Plasmon Resonance (SPR) and verified by Western blot and RT-PCR. Molecular modeling and simulation studies were used to identify a potent hit targeting Cdk5 and validated by binding studies using SPR. The peptide rescue effect was analyzed by MTT assay in the AD cellular model. SPR analysis revealed a significant change in Cdk5 and Mcl1 levels in the serum samples of AD and MCI compared to GC. Results were validated by Western blot and RT-PCR. Binary logistic regression analysis revealed that the concentration of both Cdk5 and Mcl1 was independently associated with disease after adjusting for certain parameters. ROC analysis established an optimum diagnostic cutoff value for Cdk5 [24.97 ng/µL (AUC-0.90)] and Mcl1 [23.08 ng/µL (AUC-0.94)] with high sensitivity and specificity. The peptide YCWS strongly binds to Cdk5′s ATP binding site, confirmed by molecular modeling and SPR. In the AD cellular model, peptide YCWS rescued neurotoxicity, increased Mcl1 levels, and reduced destructive hallmarks by inhibiting Cdk5. It can be concluded that Cdk5 is a promising molecule as a circulatory biomarker for the diagnosis of the early stages of AD, and its peptide inhibitor YCWS is a potential therapeutic agent. Full article
(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases: Shaping the Future of Diagnosis and Treatment)
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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 888
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)
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Review

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23 pages, 1972 KB  
Review
Detecting Alzheimer’s Disease Using Ocular Tissue and Imaging: What Do We Know?
by Minali Prasad and Manju L. Subramanian
Biomolecules 2025, 15(11), 1519; https://doi.org/10.3390/biom15111519 - 28 Oct 2025
Viewed by 718
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative condition with increasing global prevalence. As early diagnosis becomes critical for timely symptomatic management, noninvasive and easily accessible biomarkers are needed. Given the shared embryologic origins between the eye and the brain, ocular imaging has emerged [...] Read more.
Alzheimer’s disease (AD) is a progressive neurodegenerative condition with increasing global prevalence. As early diagnosis becomes critical for timely symptomatic management, noninvasive and easily accessible biomarkers are needed. Given the shared embryologic origins between the eye and the brain, ocular imaging has emerged as a promising diagnostic technique. This review summarizes the associations between AD, ocular imaging and fluid biomarkers in the anterior and posterior segment. We also describe the underlying pathophysiology that explains the connections between each ocular structure and the brain in the context of AD. Optical coherence tomography (OCT), OCT angiography, and fundus photography are the most common imaging modalities utilized in AD research. However, these techniques may or may not be feasible in primary care or neurologic clinical settings. Compared to plasma biomarker analysis, which is minimally invasive and nearing clinical implementation, ocular biomarkers remain primarily valuable in research investigations. Full article
(This article belongs to the Special Issue Biomarkers in Neurodegenerative Diseases: Shaping the Future of Diagnosis and Treatment)
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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
Cited by 1 | Viewed by 1724
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)
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