Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Neuroinflammation: Advancements in Pathophysiology and Therapies
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Neuroinflammation: Advancements in Pathophysiology and Therapies

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

Deadline for manuscript submissions: 31 August 2024 | Viewed by 1743

Special Issue Editor

Dr. David Martín-Hernández

E-Mail Website
Guest Editor
1. Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), 28029 Madrid, Spain
2. Departamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Instituto de Investigación Hospital 12 de Octubre (i+12), Instituto Universitario de Investigación en Neuroquímica (IUIN), 28040 Madrid, Spain
Interests: neuropsychopharmacology; inflammation; microbiome; glía; barrier function; psychiatric diseases; schizophrenia; depression

Special Issue Information

Dear Colleagues,

Neuroinflammation stands as a pervasive phenomenon that cuts across various conditions that affect the central nervous system (CNS), encompassing neurological, neurodegenerative, cardiovascular, and psychiatric disorders. Furthermore, neuroinflammation might also have a role in physiological processes such as aging. In essence, inflammation is a homeostatic mechanism triggered by stimuli of diverse nature to protect the organism. However, if the inflammatory process falters in eliminating potential menaces and persists over time, it can hamper normal CNS function and contribute to disease development. Despite the etiological responsibilities of neuroinflammation sparking an intense debate, its concurrence and consequences represent a harmful threat and may exacerbate the progression and severity of CNS diseases. In this context, a wealth of meta-analyses and an expanding body of clinical and preclinical data underscore the efficacy of anti-inflammatory treatments in some facets of these pathologies, supporting the fact that uncontrolled and chronic neuroinflammation endangers the CNS. Nevertheless, the precise molecular mechanisms underpinning neuroinflammation, its significance for the pathophysiology of certain diseases, and the search for novel therapies aimed at modulating neuroinflammation for clinical improvement remain limited, thereby necessitating further research.

This Special Issue aims to provide a broad overview of the latest cutting-edge advancements in neuroinflammation research, emphasizing its role in the pathophysiology of diseases and innovative treatment strategies. We welcome original research articles, reviews, brief reports, or any other contributions dealing with the following:

  • Molecular, cellular, and tissue-level mechanisms governing neuroinflammation and their regulatory pathways;
  • Neuroinflammation in the pathophysiology of CNS or systemic diseases;
  • Emerging pharmacological approaches for managing or modulating neuroinflammation.

We hope that Special Issue will serve as a trove of recent and current knowledge for newcomers and experienced scientists in this dynamic field.

Dr. David Martín-Hernández
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. 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
  • CNS diseases
  • pathophysiology
  • therapeutic strategies
  • pharmacological treatments
  • neurological disorders
  • neurodegenerative diseases
  • cardiovascular diseases
  • psychiatric disorders

Published Papers (2 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

24 pages, 7642 KiB  
Article
The Effect of Prenatal and Neonatal Fluoride Exposure to Morphine-Induced Neuroinflammation
by Patrycja Kupnicka, Joanna Listos, Maciej Tarnowski, Agnieszka Kolasa, Patrycja Kapczuk, Anna Surówka, Jakub Kwiatkowski, Kamil Janawa, Dariusz Chlubek and Irena Baranowska-Bosiacka
Int. J. Mol. Sci. 2024, 25(2), 826; https://doi.org/10.3390/ijms25020826 - 09 Jan 2024
Cited by 1 | Viewed by 988
Abstract
Physical dependence is associated with the formation of neuroadaptive changes in the central nervous system (CNS), both at the molecular and cellular levels. Various studies have demonstrated the immunomodulatory and proinflammatory properties of morphine. The resulting neuroinflammation in drug dependence exacerbates substance abuse-related [...] Read more.
Physical dependence is associated with the formation of neuroadaptive changes in the central nervous system (CNS), both at the molecular and cellular levels. Various studies have demonstrated the immunomodulatory and proinflammatory properties of morphine. The resulting neuroinflammation in drug dependence exacerbates substance abuse-related behaviors and increases morphine tolerance. Studies prove that fluoride exposure may also contribute to the development of neuroinflammation and neurodegenerative changes. Morphine addiction is a major social problem. Neuroinflammation increases tolerance to morphine, and neurodegenerative effects caused by fluoride in structures related to the development of dependence may impair the functioning of neuronal pathways, change the concentration of neurotransmitters, and cause memory and learning disorders, which implies this element influences the development of dependence. Therefore, our study aimed to evaluate the inflammatory state of selected brain structures in morphine-dependent rats pre-exposed to fluoride, including changes in cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) expression as well as microglial and astroglial activity via the evaluation of Iba1 and GFAP expression. We provide evidence that both morphine administration and fluoride exposure have an impact on the inflammatory response by altering the expression of COX-1, COX-2, ionized calcium-binding adapter molecule (Iba1), and glial fibrillary acidic protein (GFAP) in brain structures involved in dependence development, such as the prefrontal cortex, striatum, hippocampus, and cerebellum. We observed that the expression of COX-1 and COX-2 in morphine-dependent rats is influenced by prior fluoride exposure, and these changes vary depending on the specific brain region. Additionally, we observed active astrogliosis, as indicated by increased GFAP expression, in all brain structures of morphine-dependent rats, regardless of fluoride exposure. Furthermore, the effect of morphine on Iba1 expression varied across different brain regions, and fluoride pre-exposure may influence microglial activation. However, it remains unclear whether these changes are a result of the direct or indirect actions of morphine and fluoride on the factors analyzed. Full article
(This article belongs to the Special Issue Neuroinflammation: Advancements in Pathophysiology and Therapies)
►▼ Show Figures

Figure 1

Review

Jump to: Research

17 pages, 1615 KiB  
Review
Neuroinflammation and Epilepsy: From Pathophysiology to Therapies Based on Repurposing Drugs
by Pascual Sanz, Teresa Rubio and Maria Adelaida Garcia-Gimeno
Int. J. Mol. Sci. 2024, 25(8), 4161; https://doi.org/10.3390/ijms25084161 - 09 Apr 2024
Viewed by 413
Abstract
Neuroinflammation and epilepsy are different pathologies, but, in some cases, they are so closely related that the activation of one of the pathologies leads to the development of the other. In this work, we discuss the three main cell types involved in neuroinflammation, [...] Read more.
Neuroinflammation and epilepsy are different pathologies, but, in some cases, they are so closely related that the activation of one of the pathologies leads to the development of the other. In this work, we discuss the three main cell types involved in neuroinflammation, namely (i) reactive astrocytes, (ii) activated microglia, and infiltration of (iii) peripheral immune cells in the central nervous system. Then, we discuss how neuroinflammation and epilepsy are interconnected and describe the use of different repurposing drugs with anti-inflammatory properties that have been shown to have a beneficial effect in different epilepsy models. This review reinforces the idea that compounds designed to alleviate seizures need to target not only the neuroinflammation caused by reactive astrocytes and microglia but also the interaction of these cells with infiltrated peripheral immune cells. Full article
(This article belongs to the Special Issue Neuroinflammation: Advancements in Pathophysiology and Therapies)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop