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Advances in Molecular Mechanisms of Neurodegeneration and Neuroinflammation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 200

Special Issue Editors


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Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy
Interests: molecular biology; neuroinflammation; pharmacology; inflammation; oxidative stress
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Special Issue Information

Dear Colleagues,

Neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, are characterized by the progressive loss of neurons and cognitive and/or motor impairments. Mounting evidence has revealed that neuroinflammation plays a pivotal role in the onset and progression of these disorders, interacting closely with cellular and molecular events such as oxidative stress, protein aggregation, mitochondrial dysfunction, and impaired autophagy.

This Special Issue, "Advances in Molecular Mechanisms of Neurodegeneration and Neuroinflammation", aims to explore recent breakthroughs in understanding the intricate molecular pathways involved in neurodegenerative processes and inflammatory responses in the central nervous system. We invite original research articles, reviews, and short communications that focus on, but are not limited to, the roles of glial cell activation, immune signaling cascades, non-coding RNAs, epigenetic regulation, and novel therapeutic targets modulating these mechanisms.

Submissions involving in vitro, in vivo, or computational models, as well as translational studies investigating potential biomarkers or pharmacological interventions, are welcome. This Special Issue seeks to provide a platform for the latest findings that could foster the development of innovative therapeutic strategies to prevent or delay neurodegeneration and its associated pathologies.

Dr. Marika Lanza
Dr. Giovanna Casili
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 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • neuroinflammation
  • neurodegeneration
  • mitochondrial dysfunction
  • oxidative stress
  • metabolomics
  • therapeutic strategies

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Published Papers (1 paper)

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13 pages, 6907 KiB  
Article
The Characterization of the Neuroimmune Response in Primary Pterygia
by Luis Fernando Barba-Gallardo, Sofía Guadalupe Ocón-Garcia, Manuel Enrique Avila-Blanco, José Luis Diaz-Rubio, Javier Ventura-Juárez, Elizabeth Casillas-Casillas and Martín Humberto Muñoz-Ortega
Int. J. Mol. Sci. 2025, 26(15), 7417; https://doi.org/10.3390/ijms26157417 (registering DOI) - 1 Aug 2025
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Abstract
Several chronic inflammatory processes are currently being studied in relation to other systems to better understand the regulation mechanisms and identify potential therapeutic targets. A significant body of evidence supports the role of the nervous system in regulating various immunological processes. This study [...] Read more.
Several chronic inflammatory processes are currently being studied in relation to other systems to better understand the regulation mechanisms and identify potential therapeutic targets. A significant body of evidence supports the role of the nervous system in regulating various immunological processes. This study investigates the relationship between pterygia and the sympathetic nervous system, focusing on their interaction in the inflammatory response and fibrogenic process. Sixteen surgical specimens of primary pterygia and four conjunctival tissue samples were examined, and their morphology was analyzed using hematoxylin–eosin and Masson’s trichrome stains. The gene expression of adrenergic receptors, as well as inflammatory and fibrogenic cytokines, was also assessed. Additionally, both adrenergic receptors and tyrosine hydroxylase were found to be localized within the tissues according to immunohistochemistry and immunofluorescence techniques. Increased expression of proinflammatory, fibrogenic, and adrenergic genes was observed in the pterygium compared to the healthy conjunctiva. Adrenergic receptors and tyrosine hydroxylase were localized in the basal region of the epithelium and within blood vessels, closely associated with immune cells. Neuroimmunomodulation plays a key role in the pathogenesis of pterygia by activating the sympathetic nervous system. At the intravascular level, norepinephrine promotes the migration of immune cells, thereby sustaining inflammation. Additionally, sympathetic nerve fibers located at the subepithelial level contribute to epithelial growth and the fibrosis associated with pterygia. Full article
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