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Biomedicines
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Neuroinflammation: From Mechanisms to Therapeutic Approaches
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Neuroinflammation: From Mechanisms to Therapeutic Approaches

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 30 April 2027 | Viewed by 799

Editor

Dr. Yuen Gao

E-Mail Website
Guest Editor
Department of Radiology, Michigan State University, East Lansing, MI 48824, USA
Interests: bioinformatics; computational biology; artificial intelligence; brain development and disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation is now widely appreciated as a core, mechanistically informative feature of many CNS disorders, including neurodegenerative diseases, demyelinating conditions, stroke and traumatic injury, infection, and selected neuropsychiatric syndromes. Importantly, inflammatory programs in the brain are not simply downstream consequences of pathology; they can shape synaptic remodeling, neuronal vulnerability, and blood–brain barrier function through dynamic interactions among microglia, astrocytes, neurons, peripheral immune cells, and the neurovascular unit. As tools such as single-cell and spatial profiling, advanced imaging, and human genetics refine our view of inflammatory states, the field is poised to move from descriptive associations toward actionable, disease-stage-specific interventions.

This Special Issue, “Neuroinflammation: From Mechanisms to Therapeutic Approaches,” welcomes original research and authoritative reviews that bridge fundamental mechanisms with translational impact. We invite submissions addressing, for example, glial state regulation; cytokine/chemokine and complement signaling; inflammasomes, immunometabolism, and oxidative stress; neuroimmune-synaptic and neurovascular crosstalk; BBB dysfunction and systemic immune influences; biomarkers and imaging (CSF/plasma, PET, multi-omics signatures); and therapeutic strategies including anti-inflammatory and immunomodulatory agents, biologics, gene/RNA-based approaches, pro-resolving mediators, microbiome-directed interventions, and regenerative cell or cell-free therapies. By bringing together diverse experimental and clinical viewpoints, this Special Issue seeks to clarify convergent inflammatory mechanisms, highlight emerging therapeutic opportunities, and accelerate translation from discovery to patient benefit.

Dr. Yuen Gao
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines 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 2600 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
  • molecular mechanism
  • cell-free stem-cell-based therapy
  • anti-inflammation

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Published Papers (1 paper)

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Research

22 pages, 46427 KB  
Article
Quercetin Alleviates Neuroinflammation in Chronic Insomnia by Modulating the RAGE/NF-κB Signaling Pathway: Insights from Network Pharmacology and In Vitro Validation
by Guangming Liu, Nianshan Cai, Haiyi Wang, Miaomiao Liu, Wenjing Yan, Yiru Zhao, Meng Cui, Xiangpan Kong, Hongxu Sun and Peng Zhao
Biomedicines 2026, 14(8), 1766; https://doi.org/10.3390/biomedicines14081766 - 5 Aug 2026
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Abstract
Background: Chronic insomnia (CI) is increasingly recognized to be closely associated with neuroimmune dysregulation and neuroinflammation. While the dietary flavonoid quercetin exhibits known broad-spectrum anti-inflammatory properties, its specific multi-target network and underlying mechanisms concerning CI-associated neuroinflammation remain systematically unmapped. Therefore, this study [...] Read more.
Background: Chronic insomnia (CI) is increasingly recognized to be closely associated with neuroimmune dysregulation and neuroinflammation. While the dietary flavonoid quercetin exhibits known broad-spectrum anti-inflammatory properties, its specific multi-target network and underlying mechanisms concerning CI-associated neuroinflammation remain systematically unmapped. Therefore, this study integrated network pharmacology with in vitro experimental validation to elucidate the specific targets and mechanistic pathways of quercetin against neuroinflammatory responses implicated in CI. Methods: Potential targets of quercetin were predicted using the SwissTargetPrediction and SEA platforms, while CI-associated targets were curated from GeneCards, OMIM, and CTD. To bridge computational predictions with physiological relevance, protein–protein interaction (PPI) and functional enrichment analyses were integrated with molecular docking to assess the binding landscape of key candidates. Subsequently, to empirically validate these network-derived mechanistic hypotheses, in vitro experiments were conducted using an LPS-stimulated BV2 microglial model. Pro-inflammatory mediators were quantified via qRT-PCR, and the regulatory dynamics of the RAGE/NF-κB axis were evaluated by Western blotting. Results: Fifty-five overlapping targets were identified, prioritizing six hub genes (e.g., TNF, AKT1, IL6). By harmonizing the predicted network topology with experimental observations in the BV2 microglial framework, our results provide a unified mechanism linking quercetin to the suppression of central neuroinflammation. Enrichment highlighted the AGE-RAGE and IL-17 pathways as central mechanistic nodes. Molecular docking confirmed high-strength affinities between Quercetin and core targets. In the in vitro neuroinflammation model, quercetin (10, 30, and 60 μM) exerted a dose-responsive suppression of TNF-α, IL-1β, IL-6, and iNOS, while concurrently elevating anti-inflammatory IL-10 levels. Mechanistically, Quercetin significantly downregulated RAGE expression and blunted the phosphorylation of P65 and IκB, leading to significant reductions in p-P65/P65 and p-IκB/IκB ratios. Conclusions: Our findings demonstrate that Quercetin may attenuate neuroinflammatory responses associated with CI through modulation of the RAGE/NF-κB signaling axis, as indicated by network pharmacology prediction and further supported by validation in an LPS-stimulated BV2 microglial model. While these in vitro anti-inflammatory effects provide a robust mechanistic basis for targeting neuroimmune dysregulation, further in vivo behavioral studies are necessary to evaluate its direct therapeutic efficacy against chronic insomnia. Full article
(This article belongs to the Special Issue Neuroinflammation: From Mechanisms to Therapeutic Approaches)
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