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Biology
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Neurodegeneration: Pathways and Mechanisms
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Neurodegeneration: Pathways and Mechanisms

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 7305

Editors

Dr. Ferdinando Franzoni

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy
Interests: oxidative stress; brain function; neurodegeneration; antioxidant capability; physical exercise
Special Issues, Collections and Topics in MDPI journals
Dr. Giorgia Scarfò

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy
Interests: oxidative stress; brain function; neurodegeneration; antioxidant capability; physical exercise
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegeneration denotes a complex phenomenon that primarily causes the reduction in nervous cells and the loss of their function, leading to a wide range of clinical manifestations that characterize the main neurodegenerative diseases. 

Despite the phenotypic heterogeneity of these disorders, the progressive neurodegeneration is due, in most cases, to common cellular pathways, including inflammation, increased oxidative stress, altered apoptotic mechanisms, defects in autophagy and lysosomal functions, and impaired cell metabolism, as well as to a genetic predisposition.

We are pleased to invite you to the present Special Issue, whose purpose is to investigate molecular pathways affecting neurodegeneration; original research articles and reviews are welcome. 

Research areas may include (but are not limited to) the following:

  • Oxidative stress and inflammation;
  • Apoptosis, autophagy, and lysosomal function;
  • Epigenetic mechanisms affecting neurodegeneration (exercise, diet);
  • Gut–brain

We look forward to receiving your contributions.

Dr. Ferdinando Franzoni
Dr. Giorgia Scarfò
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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access semimonthly 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

  • inflammation
  • oxidative stress
  • apoptosis
  • exercise
  • diet
  • cellular pathways

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Published Papers (3 papers)

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Review

39 pages, 4271 KB  
Review
Natural Product-Derived Carbon Dots in Neurodegenerative Diseases: Advances in Blood–Brain-Barrier-Related Delivery, Neuroprotection, and Theranostics
by Kaixin Song, Xiang Gu, Na Sun, Rujia Xie, Ziyan Chen, Zili Wang, Ya Li and Lei Meng
Biology 2026, 15(15), 1235; https://doi.org/10.3390/biology15151235 - 25 Jul 2026
Viewed by 592
Abstract
The mechanisms underlying neurodegenerative diseases (NDDs) involve multiple pathological processes, such as abnormal protein aggregation, oxidative stress, neuroinflammation, mitochondrial dysfunction, and the disruption of neurovascular unit homeostasis. The blood–brain barrier (BBB) restricts drug exposure in the brain, posing a significant challenge for central [...] Read more.
The mechanisms underlying neurodegenerative diseases (NDDs) involve multiple pathological processes, such as abnormal protein aggregation, oxidative stress, neuroinflammation, mitochondrial dysfunction, and the disruption of neurovascular unit homeostasis. The blood–brain barrier (BBB) restricts drug exposure in the brain, posing a significant challenge for central nervous system delivery and for improving therapeutic efficacy. In recent years, carbon dots derived from natural products (CDs) have emerged as candidate materials for brain delivery and theranostic applications due to their small size, modifiable surfaces, fluorescence-tracking capability, and potential neuroprotective activity. This narrative review summarizes their sources, physicochemical characteristics, biological basis, interactions with the BBB, delivery strategies, neuroprotective effects, and imaging applications. Current evidence suggests that these CDs can alleviate oxidative stress and inflammatory responses, influence abnormal protein aggregation, and support drug delivery and fluorescence tracking in certain cellular and animal models. However, BBB permeability, brain fluorescence signals, brain parenchymal exposure, and therapeutic efficacy represent distinct levels of evidence and should not be considered interchangeable. Future studies should focus on strengthening material standardization, ensuring batch-to-batch consistency, characterizing absorption, distribution, metabolism, and excretion (ADME), conducting long-term safety assessments, and validating using humanized BBB models. Full article
(This article belongs to the Special Issue Neurodegeneration: Pathways and Mechanisms)
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Graphical abstract

29 pages, 1680 KB  
Review
From Inflammatory RNAs to Therapeutic Silencing: Deciphering the RNA–Inflammation Axis in Cancer and Neurodegeneration
by Emily Do, Durga Puro and Surajit Hansda
Biology 2026, 15(14), 1106; https://doi.org/10.3390/biology15141106 - 9 Jul 2026
Viewed by 524
Abstract
Inflammation is a critical protective response that maintains tissue homeostasis. However, persistent or dysregulated inflammation contributes significantly to the progression of cancer and neurodegenerative diseases. Recent advances in RNA biology have identified non-coding RNAs (ncRNAs), including microRNAs, long non-coding RNAs, and circular RNAs, [...] Read more.
Inflammation is a critical protective response that maintains tissue homeostasis. However, persistent or dysregulated inflammation contributes significantly to the progression of cancer and neurodegenerative diseases. Recent advances in RNA biology have identified non-coding RNAs (ncRNAs), including microRNAs, long non-coding RNAs, and circular RNAs, as key modulators of inflammatory signaling networks. These RNA molecules regulate key pathways such as NF-κB, STAT3, MAPK, and PI3K/AKT, thereby influencing immune responses, tumor progression, neuronal survival, and cellular stress adaptation. In parallel, RNA-sensing receptors, including Toll-like receptors and RIG-I-like receptors, connect innate immune activation with chronic inflammatory pathology. Emerging evidence further demonstrates that inflammatory RNAs participate in epigenetic regulation, intercellular communication, and inter-organ crosstalk through extracellular vesicles and exosomes. In cancer, RNA-mediated feedback loops sustain tumor-promoting inflammation, metastasis, and immune evasion, whereas in neurodegenerative disorders, they contribute to glial activation, neuronal dysfunction, and progressive neuroinflammation. This review examines the mechanistic relationship between RNA dysregulation and inflammation across cancer and neurodegeneration, with particular emphasis on RNA signaling networks, exosomal communication, and targeted RNA-based therapeutics. Collectively, advances in understanding the RNA–inflammation axis may reveal new opportunities for precision diagnostics and next generation therapeutic interventions. Full article
(This article belongs to the Special Issue Neurodegeneration: Pathways and Mechanisms)
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31 pages, 1208 KB  
Review
Melatonin as a Guardian of Mitochondria: Mechanisms and Therapeutic Potential in Neurodegenerative Diseases
by Yanyu Bao, Guoying Miao, Nannan He, Xingting Bao, Zheng Shi, Cuilan Hu, Xiongxiong Liu, Bing Wang and Chao Sun
Biology 2026, 15(2), 189; https://doi.org/10.3390/biology15020189 - 20 Jan 2026
Cited by 15 | Viewed by 5676
Abstract
Mitochondrial dysfunction is a key early pathological process in neurodegenerative diseases (NDs), leading to oxidative stress, impaired energy metabolism, and neuronal apoptosis prior to the onset of clinical symptoms. Although mitochondria represent important therapeutic targets, effective interventions targeting mitochondrial function remain limited. This [...] Read more.
Mitochondrial dysfunction is a key early pathological process in neurodegenerative diseases (NDs), leading to oxidative stress, impaired energy metabolism, and neuronal apoptosis prior to the onset of clinical symptoms. Although mitochondria represent important therapeutic targets, effective interventions targeting mitochondrial function remain limited. This review summarizes current evidence regarding the mechanisms by which melatonin protects mitochondria and evaluates its therapeutic relevance, with a primary focus on Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease—the major protagonists of NDs—while briefly covering other NDs such as amyotrophic lateral sclerosis, multiple sclerosis, and prion diseases. Melatonin selectively accumulates in neuronal mitochondria and exerts neuroprotection through multiple pathways: (1) direct scavenging of reactive oxygen species (ROS); (2) transcriptional activation of antioxidant defenses via the SIRT3 and Nrf2 pathways; (3) regulation of mitochondrial dynamics through DRP1 and OPA1; and (4) promotion of PINK1- and Parkin-mediated mitophagy. Additionally, melatonin exhibits context-dependent pleiotropy: under conditions of mild mitochondrial stress, it restores mitochondrial homeostasis; under conditions of severe mitochondrial damage, it promotes pro-survival autophagy by inhibiting the PI3K/AKT/mTOR pathway, thereby conferring stage-specific therapeutic advantages. Overall, melatonin offers a sophisticated mitochondria-targeting strategy for the treatment of NDs. However, successful clinical translation requires clarification of receptor-dependent signaling pathways, development of standardized dosing strategies, and validation in large-scale randomized controlled trials. Full article
(This article belongs to the Special Issue Neurodegeneration: Pathways and Mechanisms)
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