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Biomedicines
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Neurodegenerative Diseases: From Mechanisms to Therapeutic Approaches, 2nd Edition
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Neurodegenerative Diseases: From Mechanisms to Therapeutic Approaches, 2nd Edition

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

Deadline for manuscript submissions: 28 February 2026 | Viewed by 3997

Special Issue Editor

Dr. Marie-Lise Maddelein

E-Mail Website
Guest Editor
Institut de Pharmacologie et de Biologie Structurale, Université Toulouse III—Paul Sabatier, Toulouse, France
Interests: neurodegenerative diseases; neurons; mechanism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are characterized by the progressive degeneration of the nervous system. These diseases result in the progressive and irreversible loss of neurons, leading to cognitive decline or motor dysfunction. The best-known neurodegenerative diseases are Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).

Neurodegeneration can result from different mechanisms: (a) Protein misfolding and aggregation. Beta-amyloid peptide and tau protein have been implicated in Alzheimer's disease, alpha-synuclein in Parkinson's disease, and huntingtin in Huntington’s disease. (b) Oxidative stress damages cellular structures, including neurons, and may contribute to their degeneration. (c) Chronic inflammation within the nervous system can exacerbate neuronal damage and contribute to the progression of neurodegenerative diseases. (d) Mutations in specific genes can increase an individual’s susceptibility to developing these diseases. For example, mutations in the APP, PSEN1, and PSEN2 genes are associated with familial forms of early-onset Alzheimer's disease.

The aim of this Special Issue of Biomedicines is to present mechanisms involved in neurodegenerative diseases, or to outline therapeutic approaches with their progress and pitfalls.

Dr. Marie-Lise Maddelein
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-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

  • neurodegenerative diseases
  • neurons
  • mechanism

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Related Special Issue

Published Papers (3 papers)

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Research

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10 pages, 236 KB  
Article
The Relationship Between Systemic Inflammatory Index and Other Inflammatory Markers with Clinical Severity of the Disease in Patients with Parkinson’s Disease
by Aybala Neslihan Alagoz, Aydan Dagdas, Sena Destan Bunul and Guldeniz Cetin Erci
Biomedicines 2025, 13(8), 2029; https://doi.org/10.3390/biomedicines13082029 - 20 Aug 2025
Cited by 1 | Viewed by 1433
Abstract
Background/Objectives: Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra (SN), pathological accumulation of alpha-synuclein, and chronic neuroinflammation. The aim of this study is to evaluate the serum levels of systemic inflammatory [...] Read more.
Background/Objectives: Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra (SN), pathological accumulation of alpha-synuclein, and chronic neuroinflammation. The aim of this study is to evaluate the serum levels of systemic inflammatory markers such as neutrophil–lymphocyte ratio (NLR), neutrophil-HDL ratio (NHR), monocyte-HDL ratio (MHR), platelet–lymphocyte ratio (PLR), IL-6, IGF-1, systemic immune-inflammation index (SII), and systemic inflammation response index (SIRI) in patients with PD, and to analyze the relationship between these markers and the clinical stage of the disease as well as its motor and non-motor symptoms. Methods: Fifty-one patients diagnosed with PD and forty-nine HC matched for age and sex were evaluated prospectively. Results: NLR, NHR, and IGF-1 levels were found to be significantly higher in the PD group compared to the HC group (p < 0.05). There was no significant difference between the two groups in terms of PLR, MHR, SII, and SIRI. No significant relationship was found between the inflammatory markers and disease duration, clinical scales, or symptoms. Conclusions: These findings support the role of systemic inflammation in the pathophysiology of PD. Further multi-center, long-term follow-up studies—including simultaneous measurements of central nervous system inflammation markers—are needed for translation into clinical practice. Full article
(This article belongs to the Special Issue Neurodegenerative Diseases: From Mechanisms to Therapeutic Approaches, 2nd Edition)

Review

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18 pages, 1404 KB  
Review
Energy-Metabolic Imbalance of Oligodendrocytes in Multiple Sclerosis: Mechanisms, Network Coupling, and Advances in Metabolism-Targeted Therapies
by Zhimian Zhang, Jihe Kang, Xudong Guo, Taotao Jiang and Xiaoling Li
Biomedicines 2025, 13(12), 2880; https://doi.org/10.3390/biomedicines13122880 - 26 Nov 2025
Viewed by 530
Abstract
Oligodendrocytes (OLs), the myelin-forming cells of the central nervous system (CNS), are principal targets of autoimmune attack in multiple sclerosis (MS), resulting in demyelination and impaired neural conduction. Recent studies indicate that white matter in patients with MS exhibits increased aerobic glycolysis alongside [...] Read more.
Oligodendrocytes (OLs), the myelin-forming cells of the central nervous system (CNS), are principal targets of autoimmune attack in multiple sclerosis (MS), resulting in demyelination and impaired neural conduction. Recent studies indicate that white matter in patients with MS exhibits increased aerobic glycolysis alongside reduced oxygen consumption—a metabolic mismatch between glucose utilization and oxygen consumption—that correlates with disability accumulation. Dysregulated energy metabolism is also a central mechanism limiting remyelination in MS. In MS, this dysregulation is characterized primarily by abnormal availability of metabolic substrates entering the CNS; in turn, it disrupts glucose and lipid metabolism within OLs, leading to mitochondrial dysfunction and a diminished capacity for myelin repair. Pharmacological studies employing metabolic intermediates as interventions have shown that correcting energy-metabolism disturbances in OLs can promote remyelination and mitigate MS symptoms, highlighting the metabolic–epigenetic axis as a potential therapeutic target. Clinical and translational research further suggests that modulation of metabolic pathways may enhance remyelination and improve brain energy homeostasis. Future work should integrate metabolomics, multimodal imaging, and multi-omics approaches to map neuron–glia metabolic-coupling networks with precision and to test, in high-quality randomized controlled trials, the efficacy and safety of metabolism-targeted therapies. Full article
(This article belongs to the Special Issue Neurodegenerative Diseases: From Mechanisms to Therapeutic Approaches, 2nd Edition)
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18 pages, 769 KB  
Review
Living with Risk, Aging with Uncertainty: A Narrative Review of Health and Genetic Vulnerability in Huntington’s Disease
by Adriana V. Muñoz-Ortega, David Conde Caballero and Lorenzo Mariano Juárez
Biomedicines 2025, 13(10), 2498; https://doi.org/10.3390/biomedicines13102498 - 14 Oct 2025
Viewed by 1052
Abstract
Background/Objectives: Huntington’s disease (HD) is an autosomal dominant, neurodegenerative disorder that, because of the availability of presymptomatic genetic testing, places at-risk individuals in an anticipatory situation of great emotional, ethical, and social complexity. This review synthesizes the subjective experiences and coping strategies [...] Read more.
Background/Objectives: Huntington’s disease (HD) is an autosomal dominant, neurodegenerative disorder that, because of the availability of presymptomatic genetic testing, places at-risk individuals in an anticipatory situation of great emotional, ethical, and social complexity. This review synthesizes the subjective experiences and coping strategies of individuals aware of their genetic risk before clinical diagnosis, emphasizing the importance of patient and family narratives as critical sources of evidence for enhancing care protocols. Methods: This work is a narrative review supported by a systematic literature search. Of the 75 studies analyzed, 22 met the inclusion criteria—i.e., qualitative research, reviews, and case studies addressing emotional, cognitive, behavioral, and ethical coping mechanisms. The information was structured within a thematic matrix, and inductive coding was applied to identify recurring patterns, unresolved tensions, and gaps in the literature. Results: Presymptomatic genetic diagnosis may trigger processes of anticipatory grief, disrupt individual and familial identity, and lead to constant somatic self-monitoring. Coping strategies vary from proactive approaches—e.g., seeking information and building support networks—to narrative reframing that emphasizes acceptance and the resignification of risk. Analyzing these narratives allowed us to identify silenced ethical dilemmas and family rituals that help alleviate uncertainty—dimensions often overlooked by traditional quantitative methods. Moreover, risk awareness also impacts reproductive and care planning decisions, underscoring the importance of ongoing, context-sensitive support. Conclusions: Coping with genetic risk in Huntington’s disease extends beyond the biomedical aspects to encompass relational, ethical, and narrative dimensions. Incorporating narrative-based medicine into genetic and psychosocial counseling is crucial for identifying implicit needs and providing more empathetic, individualized care. Full article
(This article belongs to the Special Issue Neurodegenerative Diseases: From Mechanisms to Therapeutic Approaches, 2nd Edition)
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