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Microarray Analysis Revealed Inflammatory Transcriptomic Changes after LSL60101 Treatment in 5XFAD Mice Model.

Foteini Vasilopoulou1, Carmen Escolano2, Mercè Pallàs1

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Genes
|September 28, 2021
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Summary

This study shows that LSL60101, a ligand for I2-IR, can reverse neuroinflammation in a mouse model of Alzheimer's disease (AD). This suggests a potential therapeutic strategy for AD by targeting inflammatory pathways.

Keywords:
5XFADAlzheimer’s diseaseI2 imidazoline receptorsLSL60101neuroinflammationtranscriptomics

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Genetics

Background:

  • Iodine-binding immunoglobulin-related (I2-IR) proteins are dysregulated in neurodegenerative diseases like Alzheimer's disease (AD).
  • Neuroinflammation plays a critical role in the cognitive decline associated with AD.

Purpose of the Study:

  • To investigate the role of I2-IR in neuroinflammatory pathways relevant to AD.
  • To determine the effects of LSL60101, an I2-IR ligand, on inflammation-related gene expression in the 5XFAD AD mouse model.

Main Methods:

  • Utilized a qPCR array to analyze the expression of 84 inflammation-related genes in the 5XFAD mouse model treated with LSL60101.
  • Performed hierarchical clustering and Gene Ontology (GO) pathway enrichment analysis to identify affected inflammatory pathways.
  • Validated key gene expression changes using qPCR.

Main Results:

  • LSL60101 treatment altered gene expression profiles related to inflammation in the 5XFAD model, as indicated by hierarchical clustering.
  • Pathway enrichment analysis revealed significant alterations in inflammatory response, chemotaxis, and chemokine-mediated signaling pathways (clusters 2 and 3).
  • Validation confirmed that LSL60101 induced significant changes in the expression of several key inflammation-related genes.

Conclusions:

  • LSL60101 treatment demonstrates the potential to modulate neuroinflammation in the context of Alzheimer's disease.
  • These findings suggest that targeting I2-IR with ligands like LSL60101 may offer a therapeutic approach to reverse inflammatory processes in AD development.