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Editorial Board Members’ Collection Series: “Molecular Research in NeuroInflammation”
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Editorial Board Members’ Collection Series: “Molecular Research in NeuroInflammation”

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: 20 March 2025 | Viewed by 3629

Special Issue Editors

Prof. Dr. Ludmilla Morozova-Roche

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Guest Editor
Department of Medical Biochemistry and Biophysics, Umea University, 90781 Umea, Sweden
Interests: biophysics; amyloid formation; amyloid cytotoxicity; protein misfolding; amyloid-neuroinflammatory cascade; amyloid diagnostics and prognostics; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Matthew G. Frank

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Guest Editor
Department of Psychology and Neuroscience, University of Colorado Boulder, Boulder, CO 80309, USA
Interests: neuroinflammation; probiotics
Dr. Christina Piperi

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Guest Editor
Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece
Interests: neuroinflammation; neuro-oncology; neurodegeneration; epigenetics; histone modifications; signal transduction; transcription factors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation is associated with the inflammatory responses occurring in the brain and spinal cord in response to external and internal stimuli. They are linked to the production of cytokines, chemokines, alarmins, reactive oxygen species, and secondary mediators, which are produced by CNS microglia and astrocytes, endothelial cells, and peripherally derived immune cells. The initial neuroinflammatory responses lead to the immune, physiological, biochemical, and psychological consequences, which may vary depending on the disease, injury, infection, or stress as well as on the intensity and duration of these pathological processes.

Neuroinflammation and amyloid burden are the most obvious and closely interlinked pathological manifestations of Alzheimer’s, Parkinson’s and other neurodegenerative disorders. Initially, neuroinflammation was considered as a response to the neurodegeneration process; however, recent research has demonstrated that neuroinflammation could be a trigger and a key player in neurodegenerative diseases by creating a pathogenic microenvironment in the brain tissues and by this further exacerbating amyloid aggregation. In both Alzheimer’s and Parkinson’s, the affected brain tissues are characterized by damaged responses, including extensive microglial activation and a significant rise in pro-inflammatory cytokines, which sustain inflammation and exacerbate neurodegeneration.

While neuroinflammation is generally an inherently negative process, there are some responses that may be positive, and the balance of inflammatory and intrinsic repair processes influences the functional outcome or disease progression.

In this Special Issue, we welcome a very broad range of observations on the multifaceted phenomenon of neuroinflammation occurring in various ailments and protective responses and how they can be targeted in therapeutic interventions.

Prof. Dr. Ludmilla Morozova-Roche
Dr. Matthew G. Frank
Dr. Christina Piperi
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
  • microglia
  • astrocytes
  • immune cells
  • Alzheimer
  • Parkinson

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Published Papers (3 papers)

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11 pages, 1715 KiB  
Article
Roles of 4′-O-Methylalpinum Isoflavone on Activation of Microglia Induced by Oxysterols
by Yonghae Son, Miran Kim, Dongho Lee, Ryuk Jun Kwon and Koanhoi Kim
Int. J. Mol. Sci. 2024, 25(23), 12743; https://doi.org/10.3390/ijms252312743 - 27 Nov 2024
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Abstract
Microglia play a crucial role as immune cells responsible for the brain’s defense mechanisms. Similar to the actions of macrophages in the body, microglial cells elicit an inflammatory immune response in the brain. Recent papers highlight activated microglial cells as pivotal contributors to [...] Read more.
Microglia play a crucial role as immune cells responsible for the brain’s defense mechanisms. Similar to the actions of macrophages in the body, microglial cells elicit an inflammatory immune response in the brain. Recent papers highlight activated microglial cells as pivotal contributors to inflammatory responses in the brain, leading to damage to nerve tissue and the onset of Alzheimer’s disease (AD). In the brains of AD patients, elevated levels of inflammatory cytokines such as interleukin-6 (IL-6) and oxidized cholesterol metabolites (oxysterols) are observed. These factors are closely associated with inflammatory diseases in the brain. 4′-O-Methylalpinum isoflavone (mAI), derived from Cudrania tricuspidata fruit, possesses antioxidant, neuroprotective, and anti-inflammatory properties. Consequently, this study examined the effect of mAI on the expression of IL-6, a major inflammatory cytokine. The HMC3 microglial cell line was treated with oxysterols to assess the effectiveness of mAI in mitigating this inflammatory response. The results indicated that mAI inhibited the gene expression and protein secretion of IL-6 induced by 25-hydroxycholesterol (25OHChol) and 27-hydroxycholesterol (27OHChol). Furthermore, the expression of MHC class II, a marker for microglial activation, was reduced to baseline levels. These findings suggest that mAI may serve as a viable option for suppressing and treating brain inflammatory diseases induced by cholesterol oxidation products. This is achieved by curtailing the expression of the inflammatory cytokine resulting from the activation of microglial cells by immuno-oxysterol. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: “Molecular Research in NeuroInflammation”)
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20 pages, 11119 KiB  
Article
DEAD Box Helicase 24 Is Increased in the Brain in Alzheimer’s Disease and AppN-LF Mice and Influences Presymptomatic Pathology
by Michael Axenhus, Tosca Doeswijk, Per Nilsson, Anna Matton, Bengt Winblad, Lars Tjernberg and Sophia Schedin-Weiss
Int. J. Mol. Sci. 2024, 25(7), 3622; https://doi.org/10.3390/ijms25073622 - 23 Mar 2024
Viewed by 1361
Abstract
At the time of diagnosis, Alzheimer’s disease (AD) patients already suffer from significant neuronal loss. The identification of proteins that influence disease progression before the onset of symptoms is thus an essential part of the development of new effective drugs and biomarkers. Here, [...] Read more.
At the time of diagnosis, Alzheimer’s disease (AD) patients already suffer from significant neuronal loss. The identification of proteins that influence disease progression before the onset of symptoms is thus an essential part of the development of new effective drugs and biomarkers. Here, we used an unbiased 18O labelling proteomics approach to identify proteins showing altered levels in the AD brain. We studied the relationship between the protein with the highest increase in hippocampus, DEAD box Helicase 24 (DDX24), and AD pathology. We visualised DDX24 in the human brain and in a mouse model for Aβ42-induced AD pathology—AppNL-F—and studied the interaction between Aβ and DDX24 in primary neurons. Immunohistochemistry in the AD brain confirmed the increased levels and indicated an altered subcellular distribution of DDX24. Immunohistochemical studies in AppNL-F mice showed that the increase of DDX24 starts before amyloid pathology or memory impairment is observed. Immunocytochemistry in AppNL-F primary hippocampal neurons showed increased DDX24 intensity in the soma, nucleus and nucleolus. Furthermore, siRNA targeting of DDX24 in neurons decreased APP and Aβ42 levels, and the addition of Aβ42 to the medium reduced DDX24. In conclusion, we have identified DDX24 as a protein with a potential role in Aβ-induced AD pathology. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: “Molecular Research in NeuroInflammation”)
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23 pages, 7367 KiB  
Article
Enhanced Activation of the S1PR2-IL-1β-Src-BDNF-TrkB Pathway Mediates Neuroinflammation in the Hippocampus and Cognitive Impairment in Hyperammonemic Rats
by María Sancho-Alonso, Yaiza M. Arenas, Paula Izquierdo-Altarejos, Mar Martinez-Garcia, Marta Llansola and Vicente Felipo
Int. J. Mol. Sci. 2023, 24(24), 17251; https://doi.org/10.3390/ijms242417251 - 8 Dec 2023
Cited by 1 | Viewed by 1601
Abstract
Hyperammonemia contributes to hepatic encephalopathy. In hyperammonemic rats, cognitive function is impaired by altered glutamatergic neurotransmission induced by neuroinflammation. The underlying mechanisms remain unclear. Enhanced sphingosine-1-phosphate receptor 2 (S1PR2) activation in the cerebellum of hyperammonemic rats contributes to neuroinflammation. in In hyperammonemic rats, [...] Read more.
Hyperammonemia contributes to hepatic encephalopathy. In hyperammonemic rats, cognitive function is impaired by altered glutamatergic neurotransmission induced by neuroinflammation. The underlying mechanisms remain unclear. Enhanced sphingosine-1-phosphate receptor 2 (S1PR2) activation in the cerebellum of hyperammonemic rats contributes to neuroinflammation. in In hyperammonemic rats, we assessed if blocking S1PR2 reduced hippocampal neuroinflammation and reversed cognitive impairment and if the signaling pathways were involved. S1PR2 was blocked with intracerebral JTE-013, and cognitive function was evaluated. The signaling pathways inducing neuroinflammation and altered glutamate receptors were analyzed in hippocampal slices. JTE-013 improved cognitive function in the hyperammonemic rats, and hyperammonemia increased S1P. This increased IL-1β, which enhanced Src activity, increased CCL2, activated microglia and increased the membrane expression of the NMDA receptor subunit GLUN2B. This increased p38-MAPK activity, which altered the membrane expression of AMPA receptor subunits and increased BDNF, which activated the TrkB → PI3K → Akt → CREB pathway, inducing sustained neuroinflammation. This report unveils key pathways involved in the induction and maintenance of neuroinflammation in the hippocampus of hyperammonemic rats and supports S1PR2 as a therapeutic target for cognitive impairment. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: “Molecular Research in NeuroInflammation”)
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