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Research Progress in Neurodegenerative Diseases
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Research Progress in Neurodegenerative Diseases

A special issue of Diseases (ISSN 2079-9721). This special issue belongs to the section "Neuro-psychiatric Disorders".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 1503

Special Issue Editor

Dr. Christian Barbato

E-Mail Website
Guest Editor
Institute of Biochemistry and Cell Biology (IBBC), National Research Council (CNR), Via E. Ramarini, Monterotondo Scalo, 00015 Rome, Italy
Interests: NeuroCOVID-19; SARS-CoV-2; post-COVID-19 syndrome; microRNA; RNA-induced silencing complex (RISC); RNA-binding protein; neurodegenerative disease; Alzheimer’s disease; small non-coding RNA; RNA metabolism; cellular and molecular neurobiology; translational biomedicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases represent a large group of neurological disorders with heterogeneous clinical and pathological expressions, affecting specific groups of neurons, as well as specific brain areas. Several environmental and genetic factors are associated with neurodegenerative diseases, and aging has been found to be an important risk factor. The fine-tuning of the progressive loss of neurons drives nervous system dysfunction via the formation of specific neuropathological changes in the brain, including cellular inclusions, extracellular protein deposits, and the reshaping of cell morphology and neural networks. Many different forms of neurodegenerative diseases are recognized, such as Alzheimer's, Parkinson's, Huntington's, amyotrophic lateral sclerosis, multiple sclerosis, prion diseases, spongiform encephalopathies, spinocerebellar ataxias, and others. However, as recently evidenced with the neurological consequences observed in patients with COVID-19, a new disease called NeuroCOVID-19 has emerged, and it might constitute a new frontier of research. We are pleased to invite you to make a submission to this Special Issue, titled “Research progress in Neurodegenerative Diseases”.

It has a multidisciplinary emphasis on the interplay between vascular pathology, neuroinflammation, and the progression of neurodegenerative diseases—related to neurobiology and clinical studies.

This Special Issue aims to better understand all aspects of neurodegenerative diseases while also considering clinical and preclinical neuroimaging and biomarker studies, molecular and cell biology, as well as pharmacology, the microbiota gut–brain axis, and therapeutic insights, such as RNA therapy.

We accept high-quality papers in the form of brief reports, research articles, and review articles from a broad spectrum of scientific research areas, ranging from neurobiology and neuroscience to neuro-molecular medicine. All studies in neurodegenerative disease represent the exploration of a new frontier of biomedicine and the potential development of new diagnostic tests and therapies for neurodegenerative diseases.

Dr. Christian Barbato
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 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. Diseases 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 1800 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
  • neurobiology
  • Alzheimer's disease
  • Parkinson's disease
  • prion diseases
  • amyotrophic lateral sclerosis
  • NeuroCOVID-19
  • neuroimaging
  • microbiota gut-brain axis
  • RNA therapy

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Published Papers (2 papers)

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19 pages, 11123 KB  
Article
Establishment and Characterization of Behavioral Changes in the Nuclear Localization Human α-Synuclein Transgenic Mice
by Ziou Wang, Mengchen Wei, Shengtao Fan, Zheli Li, Weihu Long, Haiting Wu, Yiwei Zhang and Zhangqiong Huang
Diseases 2025, 13(8), 261; https://doi.org/10.3390/diseases13080261 - 14 Aug 2025
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Abstract
Objectives: This study aimed to establish a transgenic mouse model expressing nucleus-localized human α-synuclein (α-syn) to investigate its impact on the central nervous system and behavior and the underlying mechanisms involved. Methods: A nuclear localization sequence (NLS) was added to the end of [...] Read more.
Objectives: This study aimed to establish a transgenic mouse model expressing nucleus-localized human α-synuclein (α-syn) to investigate its impact on the central nervous system and behavior and the underlying mechanisms involved. Methods: A nuclear localization sequence (NLS) was added to the end of the human SNCA (hSNCA) gene. Subsequently, an empty vector and a mammalian lentiviral vector of the hSNCA-NLS were constructed. Transgenic mice were generated via microinjection, with genotyping and protein expression confirmed by PCR and western blotting. Only male mice were used in subsequent behavioral and molecular experiments. Immunofluorescence identified the colocalization of human α-syn with the cell nucleus in mouse brain tissues. Behavioral changes in transgenic mice were assessed using open field, rotarod, and O-maze tests. qPCR and Western blotting detected expression levels of genes and proteins related to inflammation, endoplasmic reticulum stress (ERS), and apoptosis. Bulk RNA sequencing was used to screen for differentially expressed genes and signaling pathways. Results: We successfully constructed a transgenic mouse model expressing human α-syn. Human α-syn was widely expressed in the heart, liver, spleen, kidneys, and brain of the mice, with distinct nuclear localization observed. Behavioral assessments demonstrated that, by 2 months of age, the mice exhibited motor dysfunction alongside astrocyte proliferation and neuroinflammation. At 6 months, the elevated expression of ERS-related genes (ATF6, PERK, and IRE1) and activation of the PERK-Beclin1-LC3II pathway indicated progressive ERS. By 9 months, apoptotic events had occurred, accompanied by significant anxiety-like behaviors. Bulk RNA sequencing further identified key differentially expressed genes, including IL-1α, TNF, PERK, BECLIN, GABA, IL-6α, P53, LC3II, NOS, and SPAG, suggesting their involvement in the observed pathological and behavioral phenotypes. Conclusions: The nuclear localization human α-syn transgenic mice were successfully established. These findings demonstrate that nucleus-localized α-syn induces early motor deficits, which are likely mediated by neuroinflammation, whereas later anxiety-like behaviors may result from ERS-induced apoptosis. This model provides a valuable tool for elucidating the role of nuclear α-syn in Parkinson’s disease and supports further mechanistic and therapeutic research. Full article
(This article belongs to the Special Issue Research Progress in Neurodegenerative Diseases)
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10 pages, 587 KB  
Brief Report
Possible Significance of Neutrophil–Hemoglobin Ratio in Differentiating Progressive Supranuclear Palsy from Depression: A Pilot Study
by Michał Markiewicz, Natalia Madetko-Alster, Dagmara Otto-Ślusarczyk, Karolina Duszyńska-Wąs, Bartosz Migda, Patryk Chunowski, Marta Struga and Piotr Alster
Diseases 2025, 13(4), 119; https://doi.org/10.3390/diseases13040119 - 18 Apr 2025
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Abstract
Background: Research has associated chronic inflammation with the evolution of neurological and psychiatric disorders. Neurodegenerative diseases, including Parkinson’s Disease (PD), Alzheimer’s Disease (AD), and less common ones such as Progressive Supranuclear Palsy (PSP), are commonly linked to depression. However, the pathomechanisms and the [...] Read more.
Background: Research has associated chronic inflammation with the evolution of neurological and psychiatric disorders. Neurodegenerative diseases, including Parkinson’s Disease (PD), Alzheimer’s Disease (AD), and less common ones such as Progressive Supranuclear Palsy (PSP), are commonly linked to depression. However, the pathomechanisms and the role of neuroinflammation in these disorders remain unclear; therefore, interest is increasing in easily accessible inflammatory morphological assessments of blood samples, such as the neutrophil-to-lymphocyte ratio (NLR), the neutrophil-to-monocyte ratio (NMR), and the neutrophil-to-hemoglobin ratio (N/HGBR). Methods: The authors analyzed 15 age-matched controls and 21 patients with PSP; the PSP group was additionally divided into 11 patients without depression (PSP) and 10 with depression (Beck Depression Inventory [BDI] ≥ 14) (PSP-D). Results: In the PSP-D group, the level of N/HGBR was significantly lower than in the controls (p = 0.01), but there were no significant differences in any other neutrophil-derived parameters or comparisons of morphological blood assessment. Patients with PSP-D exhibited a marginally significant decrease in neutrophil levels compared to the controls. Conclusions: This is the first study highlighting the possible significance of peripheral inflammatory factors in patients with PSP affected by depression. It highlights possible tendencies in the area of non-specific inflammatory markers and suggests their relation to affective disorders in PSP. Full article
(This article belongs to the Special Issue Research Progress in Neurodegenerative Diseases)
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