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Cells
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Advances in the Study of Neuroinflammation
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Advances in the Study of Neuroinflammation

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 2312

Special Issue Editor

Prof. Dr. Lars Ove Brandenburg

E-Mail Website
Guest Editor
1. Institute of Anatomy, Rostock University Medical Center, 18057 Rostock, Germany
2. Department of Anatomy and Cell Biology, RWTH Aachen University, 52062 Aachen, Germany
Interests: neuroinflammation; neurodegeneration; bacterial meningitis; antimicrobial peptides; Alzheimer’s disease; multiple sclerosis; glia cells; pattern recognition receptors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

For some time, it has been known that neuroinflammation is a complex multicellular process that plays a central role in a variety of neurological diseases, including acute inflammation, such as bacterial meningitis, as well as chronic inflammation in the form of neurodegenerative diseases or psychiatric and immune-mediated disorders. Numerous findings indicate that neuroinflammation can promote the progression of these disorders. In particular, the function of glial cells (astrocytes and microglial cells) and their activation, as well as the connection with immigrated immune cells in disease, are of great interest. The blood–brain barrier and the lymphatic pathways, as important sites of communication between the periphery and the CNS, have also become the focus of scientific investigations. As a result, there has been an explosion of interest in neuroinflammation and the tools available to study these processes in the brain.

This Special Issue seeks papers covering a wide range of topics related to studies of acute or chronic neuroinflammation, which show the developments of new models or therapeutic approaches and new objects, as well as the roles of interesting factors and glial cells in various disorders.

The article, which can focus on a topic of your choice, can be written in the form of a comprehensive review, an original article, or another type of article.

Prof. Dr. Lars Ove Brandenburg
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. Cells 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

  • neuroinflammation
  • neurodegenerative disease
  • bacterial meningitis
  • glia cell
  • microglial cell
  • macrophage
  • astrocyte
  • blood–brain barrier
  • meninges
  • meningeal immunity
  • meningeal lymphatic vessels

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Related Special Issue

Published Papers (2 papers)

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Research

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13 pages, 2309 KiB  
Article
The Formyl Peptid Receptor Ligand Ac2-26 Improves the Integrity of the Blood−Brain Barrier in the Course of Pneumococcal Meningitis
by Johannes Deutloff, Irina Pöhner, Johann Rößler, Markus Kipp, Simone C. Tauber and Lars-Ove Brandenburg
Cells 2024, 13(24), 2104; https://doi.org/10.3390/cells13242104 - 19 Dec 2024
Viewed by 702
Abstract
Background: The brain is protected from invading pathogens by the blood−brain barrier (BBB) and the innate immune system. Pattern recognition receptors play a crucial role in detecting bacteria and initiating the innate immune response. Among these are G-protein-coupled formyl peptide receptors (FPR), which [...] Read more.
Background: The brain is protected from invading pathogens by the blood−brain barrier (BBB) and the innate immune system. Pattern recognition receptors play a crucial role in detecting bacteria and initiating the innate immune response. Among these are G-protein-coupled formyl peptide receptors (FPR), which are expressed by immune cells in the central nervous system. In this study, we investigated the influence of the FPR ligand Ac2-26 on the integrity of the BBB during pneumococcal meningitis. Methods: Wild-type (WT) and Fpr1- and Fpr2-deficient mice were intrathecally infected with Streptococcus pneumoniae. Subsequently, different groups of mice were treated with intraperitoneal injections of Ac2-26. The integrity of the BBB was analyzed using various markers through immunohistochemistry and immunofluorescence. Results: The results showed reduced BBB integrity during the course of bacterial meningitis. Treatment with Ac2-26 in WT mice significantly prolonged the maintenance of BBB integrity. However, this effect was not observed in Fpr2-deficient mice. Conclusions: This study extends previous findings on the anti-inflammatory properties of Ac2-26 by demonstrating that Ac2-26 positively affects BBB integrity via FPR2 during pneumococcal meningitis. These findings suggest that further investigation of Ac2-26 and other FPR modulators as potential therapies for Streptococcus pneumoniae-induced meningitis is warranted. Full article
(This article belongs to the Special Issue Advances in the Study of Neuroinflammation)
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Review

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35 pages, 2461 KiB  
Review
Modulating Neuroinflammation as a Prospective Therapeutic Target in Alzheimer’s Disease
by Eunshil Lee and Yongmin Chang
Cells 2025, 14(3), 168; https://doi.org/10.3390/cells14030168 - 22 Jan 2025
Viewed by 1204
Abstract
The recent approval of lecanemab highlights that the amyloid beta (Aβ) protein is an important pathological target in Alzheimer’s disease (AD) and further emphasizes the significance of neuroinflammatory pathways in regulating Aβ accumulation. Indeed, Aβ accumulation triggers microglia activation, which are key mediators [...] Read more.
The recent approval of lecanemab highlights that the amyloid beta (Aβ) protein is an important pathological target in Alzheimer’s disease (AD) and further emphasizes the significance of neuroinflammatory pathways in regulating Aβ accumulation. Indeed, Aβ accumulation triggers microglia activation, which are key mediators in neuroinflammation. The inflammatory responses in this process can lead to neuronal damage and functional decline. Microglia secrete proinflammatory cytokines that accelerate neuronal death and release anti-inflammatory cytokines and growth factors contributing to neuronal recovery and protection. Thus, microglia play a dual role in neurodegeneration and neuroprotection, complicating their function in AD. Therefore, elucidating the complex interactions between Aβ protein, microglia, and neuroinflammation is essential for developing new strategies for treating AD. This review investigates the receptors and pathways involved in activating microglia and aims to enhance understanding of how these processes impact neuroinflammation in AD, as well as how they can be regulated. This review also analyzed studies reported in the existing literature and ongoing clinical trials. Overall, these studies will contribute to understanding the regulatory mechanisms of neuroinflammation and developing new therapies that can slow the pathological progression of AD. Full article
(This article belongs to the Special Issue Advances in the Study of Neuroinflammation)
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