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Basic Science and Pathogenesis.

Ramon Bertoldi de Souza1, Christian Limberger1, Gabriel Colissi Martins1

  • 1Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.

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Alzheimer's disease (AD) models show varied astrocyte subtype profiles. Glutamatergic astrocytes are enriched in APP/PS1 and hAβKI models but not 5xFAD, suggesting impaired function in AD.

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Area of Science:

  • Neuroscience
  • Glial Cell Biology
  • Alzheimer's Disease Research

Background:

  • Astrocytes, crucial for brain homeostasis, display heterogeneity and altered responses in Alzheimer's disease (AD).
  • Glutamate excitotoxicity, a key AD feature, involves impaired astrocytic glutamate uptake.
  • A specific astrocyte subtype involved in glutamatergic gliotransmission has been identified.

Purpose of the Study:

  • To investigate alterations in the transcriptional profile of glutamatergic gliotransmission-specialized astrocytes across different AD mouse models.
  • To compare the enrichment and gene expression of this astrocyte subtype in APP/PS1, 5xFAD, and hAβKI models.

Main Methods:

  • Differential gene expression analysis and cellular deconvolution (PSEA) on bulk RNA-seq data from hippocampus of three AD mouse models.
  • Assignment of cell type-specific gene signatures using the BRETIGEA R package.
  • Analysis of cellular enrichment proportions and differentially expressed genes (DEGs) within the glutamatergic astrocyte signature.

Main Results:

  • Glutamatergic astrocyte enrichment varied significantly: APP/PS1 (24.8%), hAβKI (23.8%), and 5xFAD (2.2%).
  • DEGs analysis revealed substantial gene expression changes, with notable downregulation of genes like KIF5B and GRASP, indicating impaired vesicle homeostasis.
  • The specific DEGs profiles differed across the three AD models.

Conclusions:

  • The glutamatergic astrocyte signature is distinct across AD mouse models, with differential enrichment.
  • The 5xFAD model shows minimal representation of this astrocyte subtype compared to APP/PS1 and hAβKI models.
  • Downregulation of vesicle trafficking genes suggests impaired glutamatergic astrocyte function in AD pathogenesis, warranting further investigation.