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Integrated Multi-Omics Profiling Identifies CD84-Associated Microglial Alterations in Focal Cortical Dysplasia Type

Yubao Fang1, Shengyu Yang1, Lei Lei1

  • 1Department of Neurology, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, Guangdong, People's Republic of China.

Journal of Inflammation Research
|March 20, 2026
PubMed
Summary

Focal cortical dysplasia type II (FCDII) involves neuroinflammation. This study found CD84 glycoprotein is upregulated in FCDII microglia, suggesting a role in inflammatory signaling and cell interactions.

Keywords:
CD84focal cortical dysplasia type IImicroglial activationmulti-omics integrationneuroinflammation

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genomics

Background:

  • Focal cortical dysplasia type II (FCDII) is a leading cause of pediatric drug-resistant epilepsy.
  • Its molecular underpinnings, particularly the role of neuroinflammation, are not fully understood.

Purpose of the Study:

  • To investigate the molecular pathology of FCDII using an integrated multi-omics approach.
  • To identify key molecular players, such as CD84, involved in FCDII pathogenesis.

Main Methods:

  • Employed data-independent acquisition mass spectrometry (DIA-MS) proteomics and analyzed public transcriptomic datasets.
  • Utilized protein-protein interaction (PPI) network analysis, quantitative real-time PCR (qPCR), and single-cell RNA sequencing (scRNA-seq).

Main Results:

  • Identified 460 differentially expressed proteins (DEPs) in FCDII, enriched in inflammation and development pathways.
  • Found CD84 glycoprotein consistently upregulated in FCDII, localized to a pro-inflammatory microglial subpopulation.
  • Observed increased predicted interactions between CD84-positive microglia and other brain cells.

Conclusions:

  • Suggests a role for CD84 in modulating microglial inflammation and intercellular communication in FCDII.
  • Provides preliminary molecular insights into microglial dysfunction in FCDII for future research.