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Basic Science and Pathogenesis.

Lavinia Perquim1, Marco Antônio De Bastiani1, Oak Hatzimanolis2

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Summary
This summary is machine-generated.

Dysregulated circular RNAs (circRNAs) increase with disease severity in a mouse model of Alzheimer's disease (AD). These findings reveal conserved regulatory networks impacting AD-related genes, offering insights into disease mechanisms.

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Area of Science:

  • Genomics
  • Neuroscience
  • Molecular Biology

Background:

  • Non-coding RNAs, including circRNAs and miRNAs, are crucial gene expression regulators.
  • Aberrant expression of circRNAs and miRNAs is implicated in Alzheimer's disease (AD) pathogenesis.
  • The hippocampus, a brain region vulnerable to AD, is investigated for circRNA alterations.

Purpose of the Study:

  • To assess circRNA transcription changes in the hippocampus of a transgenic AD mouse model.
  • To explore the integrated regulatory roles of circRNAs, miRNAs, and mRNAs in AD.
  • To identify conserved circRNAs and their downstream targets relevant to AD.

Main Methods:

  • Analysis of hippocampal circRNAs from APPswe/PSEN1dE9 mice at 4, 6, and 8 months using NCBI datasets.
  • CircRNA identification via CIRI2 algorithm and differential expression analysis using DESeq2 (p<0.01).
  • Construction of circRNA-miRNA regulatory networks (circFunBase) and miRNA-mRNA interactions (miRDB), followed by Gene Ontology (GO) enrichment analysis.

Main Results:

  • Identification of 41, 82, and 425 differentially expressed circRNAs at 4, 6, and 8 months, respectively.
  • 18 circRNAs were consistently altered across age groups, including circRNA HOMER1, which interacted with 36 miRNAs.
  • These miRNAs targeted 1682 genes, with GO analysis revealing 51 associated ontologies relevant to AD pathophysiology.

Conclusions:

  • CircRNA dysregulation escalates with disease progression in the APPswe/PSEN1dE9 model, mirroring human findings.
  • The study highlights conserved circRNAs and their regulatory interactions with miRNAs and mRNAs.
  • Identified pathways include neural differentiation, GABAergic signaling, stress response, and neuroinflammation, offering insights into AD mechanisms in vulnerable brain regions.