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Novel Insights into Microglia Heterogeneity and Neurodegeneration

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 October 2025 | Viewed by 739

Special Issue Editor

Special Issue Information

Dear Colleagues,

Microglia, resident immune cells in the central nervous system (CNS), play various biologically important roles under homeostatic and disease conditions, such as supporting neuronal development, synaptic pruning or scavenging dying cells. Moreover, as effector cells, microglia can influence the progress of many brain diseases, including as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis and affective disorders.

A microglial phenotype, rarely present in steady-state conditions but abundant during chronic stress, aging and Alzheimer’s disease, is represented by “dark microglia”, suggesting a new phenotype involved in the pathological remodeling of neuronal circuits, especially at the synapse level. The heterogeneity of microglia in different regions of the CNS during development, homeostasis and neurological disorders has not been fully studied and little information is known about the subgroups of microglia during disease. The main reasons for this limited knowledge include important technical limitations that do not allow for an adequate spatial and temporal representation of microglia multiplicity at the single-cell level. Previous single-cell level analyses of microglia, such as flow cytometry, in situ hybridization or immunohistochemistry, were limited to probing a few selected proteins or RNAs, which clearly hindered the ability to study complete landscapes of microglial diversity.

In this Special Issue, we aim to bring together the most recent studies exploring microglial heterogeneity using new advanced technologies to understand the role of microglia heterogeneity during development, homeostasis and in neurological disorders.

Prof. Dr. Maria Anttonietta Panaro
Guest Editor

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Keywords

  • microglia
  • synapses
  • stress
  • aging
  • heterogeneity
  • CNS
  • single-cell RNA sequencing
  • neurodegenerative diseases

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Published Papers (1 paper)

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Research

18 pages, 6905 KiB  
Article
Paeonol Relieves Chronic Neuropathic Pain by Reducing Communication Between Schwann Cells and Macrophages in the Dorsal Root Ganglia After Injury
by Xin Li, Zifeng Zhuang, Yuting Hao, Shaozi Lin, Junyan Gu, Shiquan Chang, Lin Lan, Guoping Zhao and Di Zhang
Int. J. Mol. Sci. 2025, 26(9), 3964; https://doi.org/10.3390/ijms26093964 - 22 Apr 2025
Viewed by 281
Abstract
This study investigated the mechanism underlying Paeonol’s therapeutic efficacy against neuropathic pain. GSE158892 dataset data were used to conduct a scRNA-seq analysis. In cell experiments, Schwann cells and macrophages were utilized to examine pain pathogenesis using specific inhibitors. Thirty-two SD rats were randomly [...] Read more.
This study investigated the mechanism underlying Paeonol’s therapeutic efficacy against neuropathic pain. GSE158892 dataset data were used to conduct a scRNA-seq analysis. In cell experiments, Schwann cells and macrophages were utilized to examine pain pathogenesis using specific inhibitors. Thirty-two SD rats were randomly divided into four groups: sham, chronic constriction injury (CCI), ibuprofen, and Paeonol. Behavioral tests combined with ELISA, PCR, western blot, immunohistochemistry, and immunofluorescence analyses were conducted. CellChat analysis demonstrated that, following peripheral nerve injury, Schwann cells secreted IL-34, which interacted with CSF1R on macrophages, leading to the infiltration and activation of macrophages. Paeonol reduced IL-34 production by Schwann cells induced with LPS. Conditioned medium from LPS-stimulated Schwann cells treated with Paeonol did not cause macrophage proliferation or migration, activation of the CSF1 pathway, or ROS production. In CCI rats, Paeonol alleviated mechanical and cold hyperalgesia, while reducing the production of serum inflammatory mediators. Additionally, Paeonol decreased the expression levels of IL-34, CSF1R, phosphorylated ERK (p-ERK), phosphorylated NF-κB (p-NF-κB), and components of the NLRP3 inflammasome in the dorsal root ganglia of CCI rats. Conclusion: Alleviation of neuropathic pain by Paeonol treatment may be achieved by inhibiting the IL-34–CSF1R interaction, suppressing Schwann cell–macrophage interactions, and reducing DRG neuroinflammation. Full article
(This article belongs to the Special Issue Novel Insights into Microglia Heterogeneity and Neurodegeneration)
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