Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
4.5
Journals
Biomedicines
Special Issues
Multidisciplinary Approaches to Neurodegenerative Disorders
share announcement

Multidisciplinary Approaches to Neurodegenerative Disorders

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 5685

Editor

Prof. Dr. Toomas Toomsoo

E-Mail Website
Guest Editor
1. Confido Medical Centre, Tallinn, Estonia
2. School of Natural Sciences and Health, Tallinn University, Tallinn, Estonia
Interests: neurodegenerative diseases; brain health preservation; Parkinson's disease; integrative medicine approaches; early detection and prevention

Special Issue Information

Dear Colleagues,

This Special Issue explores innovative multidisciplinary approaches to understanding, diagnosing, and treating neurodegenerative disorders. As these complex conditions continue to pose significant global health challenges, integration across disciplines has become essential for meaningful progress.

We welcome contributions bridging traditional boundaries between neuroscience, genetics, biomedical engineering, computational biology, and clinical medicine. The Special Issue seeks papers highlighting novel research methodologies, technological breakthroughs in early detection, therapeutic innovations, and emerging paradigms in disease modelling.

Key areas of interest include the following:

  • Comorbid conditions in neurodegenerative diseases—examining how multiple pathologies interact and influence disease progression.
  • Similarities and differences across neurodegenerative disorders—identifying common pathophysiological mechanisms and disease-specific features.
  • Connections between super-agers and lipid metabolism—exploring how lipid homeostasis relates to successful aging and neurodegeneration resistance.
  • Lipid metabolism alterations in neurodegenerative diseases—investigating metabolic dysfunction as both a cause and consequence of neurodegeneration.

Particular emphasis will be placed on translational research connecting fundamental molecular mechanisms to clinical applications, personalized medicine approaches, and cutting-edge interventions, including gene therapy, stem cell applications, and AI-driven diagnostic tools. We especially encourage submissions addressing how comorbidity patterns inform disease classification and treatment strategies, and how understanding metabolic signatures, particularly lipid profiles, can advance biomarker development and therapeutic targeting.

By showcasing diverse perspectives and collaborative frameworks, this Special Issue aims to catalyse new directions in neurodegenerative disease research and accelerate the development of effective interventions for conditions such as Alzheimer's, Parkinson's, ALS, and related disorders.

Prof. Dr. Toomas Toomsoo
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 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-anonymized 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

  • neurodegenerative disorders
  • lipid metabolism
  • comorbidity patterns super-agers
  • precision medicine
  • biomarker discovery
  • AI-assisted diagnostics
  • translational neuroscience
  • multi-omics integration
  • neuroinflammation

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 (3 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

63 pages, 23065 KB  
Article
Hierarchical Network Organization and Dynamic Perturbation Propagation in Autism Spectrum Disorder: An Integrative Machine Learning and Hypergraph Analysis Reveals Super-Hub Genes and Therapeutic Targets
by Larissa Margareta Batrancea, Ömer Akgüller, Mehmet Ali Balcı and Lucian Gaban
Biomedicines 2026, 14(1), 137; https://doi.org/10.3390/biomedicines14010137 - 9 Jan 2026
Viewed by 938
Abstract
Background/Objectives: Autism spectrum disorder (ASD) exhibits remarkable genetic heterogeneity involving hundreds of risk genes; however, the mechanism by which these genes organize within biological networks to contribute to disease pathogenesis remains incompletely understood. This study aims to elucidate these organizational principles and identify [...] Read more.
Background/Objectives: Autism spectrum disorder (ASD) exhibits remarkable genetic heterogeneity involving hundreds of risk genes; however, the mechanism by which these genes organize within biological networks to contribute to disease pathogenesis remains incompletely understood. This study aims to elucidate these organizational principles and identify critical network bottlenecks using a novel integrative computational framework. Methods: We analyzed 893 SFARI genes using a three-pronged computational approach: (1) a Machine Learning Dynamic Perturbation Propagation algorithm; (2) a hypergraph construction method explicitly modeling multi-gene complexes by integrating protein–protein interactions, co-expression modules, and curated pathways; and (3) Hypergraph Neural Network embeddings for gene clustering. Validation was performed using hub-independent features to address potential circularity, followed by a druggability assessment to prioritize therapeutic targets. Results: The hypergraph construction captured 3847 multi-way relationships, representing a 45% increase in biological relationships compared to pairwise networks. The perturbation algorithm achieved a 51% higher correlation with TADA genetic evidence than random walk methods. Analysis revealed a hierarchical organization where 179 hub genes exhibited a 3.22-fold increase in degree centrality and a 4.71-fold increase in perturbation scores relative to non-hub genes. Hypergraph Neural Network clustering identified five distinct gene clusters, including a “super-hub” cluster of 10 genes enriched in synaptic signaling (4.2-fold) and chromatin remodeling (3.9-fold). Validation confirmed that 8 of these 10 genes co-cluster even without topological information. Finally, we identified high-priority therapeutic targets, including ARID1A, POLR2A, and CACNB1. Conclusions: These findings establish hierarchical network organization principles in ASD, demonstrating that hub genes maintain substantially elevated perturbation states. The identification of critical network bottlenecks and pharmacologically tractable targets provides a foundation for understanding autism pathogenesis and developing precision medicine approaches. Full article
(This article belongs to the Special Issue Multidisciplinary Approaches to Neurodegenerative Disorders)
►▼ Show Figures

Figure 1

Review

Jump to: Research

18 pages, 707 KB  
Review
Clonal Hematopoiesis of Indeterminate Potential as an Emerging Interdisciplinary Risk Factor in Alzheimer’s Disease: Current Evidence and Future Directions
by Klara Kopp, Patricia Silva, Frederik Damm and Nicoleta Carmen Cosma
Biomedicines 2026, 14(5), 1012; https://doi.org/10.3390/biomedicines14051012 - 29 Apr 2026
Viewed by 688
Abstract
Clonal hematopoiesis of indeterminate potential (CHIP) is an age-related condition affecting over 10–20% of individuals older than 70 years, characterized by the expansion of hematopoietic stem cell clones carrying somatic mutations in leukemia-associated driver genes in the absence of overt hematologic disease. Initially [...] Read more.
Clonal hematopoiesis of indeterminate potential (CHIP) is an age-related condition affecting over 10–20% of individuals older than 70 years, characterized by the expansion of hematopoietic stem cell clones carrying somatic mutations in leukemia-associated driver genes in the absence of overt hematologic disease. Initially recognized as a precursor to hematologic malignancies, CHIP has since been implicated in diverse non-malignant disorders, notably increasing the risk of cardiovascular events by 40%. Recent epidemiological and experimental evidence suggests a potential disease-modifying influence of CHIP in neurodegenerative diseases, particularly Alzheimer’s disease (AD), although findings remain heterogeneous and sometimes contradictory. This review synthesizes recent evidence linking CHIP to AD risk, neuropathology, and disease progression. In this study, we summarize population-based cohort studies reporting a 36 to 54% reduction in the odds of clinical AD among CHIP carriers, alongside emerging data indicating that DNMT3A and TET2 mutations may exert divergent effects on neurodegeneration. Mechanistic insights from experimental models are examined, highlighting the ability of mutated myeloid cells to infiltrate the central nervous system and modulate neuroinflammation and amyloid clearance. We discuss conflicting findings and analyze how CHIP-driven vascular disease and stroke confound neuroprotective signals. We propose that CHIP may differentially influence AD and vascular contributions to cognitive impairment and dementia, shaping mixed dementia phenotypes. Methodological challenges, including survivor bias, competing risks, variable mutation detection thresholds, and incomplete Apolipoprotein E stratification, are discussed. Ultimately, our review clarifies that CHIP is not a simple protective factor, but a complex systemic modulator that reshapes the neurodegenerative and vascular drivers of cognitive decline, necessitating cross-disciplinary neuro-hematology collaboration to establish its role as a novel risk stratificator for improving diagnostic precision and personalizing clinical outcomes in Alzheimer’s disease. Full article
(This article belongs to the Special Issue Multidisciplinary Approaches to Neurodegenerative Disorders)
►▼ Show Figures

Figure 1

17 pages, 703 KB  
Review
Neuroplasticity Across the Autism–Schizophrenia Continuum
by Evangelia Kesidou, Nikolaos Mitsoudis, Olympia Damianidou, Charilaos Taloumtzis, Marianna Tsakiridou, Eleni Polyzoidou, Eleni Grigoriadou, Christos Bakirtzis, Evangelia Spandou and Constantina Simeonidou
Biomedicines 2025, 13(11), 2695; https://doi.org/10.3390/biomedicines13112695 - 2 Nov 2025
Cited by 2 | Viewed by 3407
Abstract
Plasticity is a fundamental property of the brain that enables the nervous system to respond appropriately to internal and external stimuli. It primarily involves changes at the synaptic level, mediated by a wide array of molecules, ultimately leading to cognitive and behavioral changes. [...] Read more.
Plasticity is a fundamental property of the brain that enables the nervous system to respond appropriately to internal and external stimuli. It primarily involves changes at the synaptic level, mediated by a wide array of molecules, ultimately leading to cognitive and behavioral changes. This review critically contrasts the developmental timing and mechanisms of plasticity in Autism spectrum disorder (early hyperplasticity and excitation–inhibition imbalance) versus Schizophrenia (adolescent overpruning and NMDAR hypofunction) and evaluates evidence for interventions that harness plasticity to improve cognitive and behavioral outcomes. Preclinical and small clinical studies suggest that interventions targeting plasticity-related pathways may improve specific cognitive and behavioral domains. However, effects appear to be symptom-domain-specific and protocol-dependent and larger randomized controlled trials are needed to confirm efficacy. Cognitive remediation for Schizophrenia has been associated with improved executive function and increased hippocampal volume, while virtual reality-based training for Autism spectrum disorder has shown gains in attention and planning skills. By highlighting both molecular mechanisms and therapeutic strategies, this review aims to provide an integrated perspective on how plasticity-targeted interventions could be optimized across neurodevelopmental and neuropsychiatric disorders. Full article
(This article belongs to the Special Issue Multidisciplinary Approaches to Neurodegenerative Disorders)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop