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Molecular Insights into Microglia in Neurological Diseases

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 August 2026 | Viewed by 1426

Special Issue Editor


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Guest Editor
Department of Biomedical Laboratory Science, Konyang University, Daejeon 35365, Republic of Korea
Interests: microglia; neurological diseases; neuroinflammation; engineered stem cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to advance our understanding of the molecular mechanisms by which microglia contribute to the onset and progression of neurological diseases. It welcomes original research and review articles that explore molecular signaling pathways regulating microglial activation in central nervous system (CNS) disorders, such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Studies addressing microglia-mediated neuroinflammation, their impact on neuronal survival and synaptic function, and the cellular interactions between microglia and neurons, astrocytes, or oligodendrocytes under pathological conditions are of particular interest. Contributions focusing on molecular imaging, biomarker development to monitor microglial activity, and therapeutic strategies targeting microglial functions are also encouraged. Additionally, research into genetic and epigenetic regulation of microglial behavior in disease models is highly relevant to the scope of this Special Issue.

Prof. Dr. Pyung-Hwan Kim
Guest Editor

Manuscript Submission Information

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Keywords

  • microglia
  • neuroinflammation
  • neurodegenerative diseases
  • molecular signaling
  • central nervous system (CNS)

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Published Papers (1 paper)

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Research

21 pages, 1959 KB  
Article
Targeting Adipocyte Enhancer-Binding Protein 1 to Induce Microglial Phenotype Shift for Immunotherapy in Alzheimer’s Disease
by Eun-Ji Kim, Byeong-Hyeon Kim, Ye-Bin Mun, Minho Moon and Pyung-Hwan Kim
Int. J. Mol. Sci. 2026, 27(1), 296; https://doi.org/10.3390/ijms27010296 - 27 Dec 2025
Viewed by 797
Abstract
Neuroinflammation, a key contributor to neurodegenerative diseases, results from excessive microglial activation. Microglia that respond to pathogenic molecules switch to the M1 type and secrete various immune cytokines, which can cause neuronal damage. Therefore, our study focused on molecules that can enhance the [...] Read more.
Neuroinflammation, a key contributor to neurodegenerative diseases, results from excessive microglial activation. Microglia that respond to pathogenic molecules switch to the M1 type and secrete various immune cytokines, which can cause neuronal damage. Therefore, our study focused on molecules that can enhance the neuroprotective role of microglia and reduce neuronal damage. The adipocyte enhancer-binding protein 1 (AEBP1) gene is known for its role in regulating immune responses in macrophages. However, its role in neuroinflammation has not been fully explored. Therefore, we investigated the role of AEBP1 in microglial cells activated by lipopolysaccharide (LPS). First, we confirmed that AEBP1 is expressed in LPS-activated microglia and demonstrated that downregulation of AEBP1 using shRNA in activated microglia reduced the immune response via the nuclear factor-kappa-B (NFκB) pathway. These results promote a shift toward neuroprotective M2 microglia, thereby reducing neuronal damage. Next, we confirmed that the expression of AEBP1 was elevated in the brains of Alzheimer’s disease (AD) mice. Additionally, animal experiments to assess the therapeutic effects of AEBP1 showed that microglia gathered around amyloid beta (Aβ) and reduced its size. Taken together, our results provide the first evidence that AEBP1 can reduce inflammatory activity in microglia, suggesting its potential as a target molecule for immunotherapy. Full article
(This article belongs to the Special Issue Molecular Insights into Microglia in Neurological Diseases)
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