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Basic Science and Pathogenesis.

Rodrigo Sebben Paes1, Gabriela Mantovani Baldasso1, Christian Limberger1

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

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Summary
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Familial Alzheimer's disease (fAD) mouse models show greater transcriptional changes than late-onset AD (LOAD) models. Neurons are consistently vulnerable across all Alzheimer's disease (AD) subtypes, indicating distinct cellular roles in disease progression.

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Late-onset Alzheimer's disease (LOAD) and familial Alzheimer's disease (fAD) may have distinct pathophysiological pathways and cellular features.
  • Understanding the role of individual brain cell types in different Alzheimer's disease (AD) subtypes is crucial.
  • Genetically modified mouse models offer valuable tools for investigating AD genetic variability.

Purpose of the Study:

  • To investigate the transcriptional signatures of hippocampal cell types across two fAD mouse models (APP/PS1, 3xTg) and one LOAD mouse model (hAß-KI).
  • To identify differentially expressed genes (DEGs) specific to neurons, astrocytes, microglia, oligodendrocytes, and endothelial cells in each model.
  • To perform functional enrichment analysis of biological processes affected in each cell type and AD model.

Main Methods:

  • Analysis of bulk hippocampal transcriptomics data from public repositories (Gene Expression Omnibus, AMP-AD Knowledge Portal).
  • Gene expression deconvolution using Population-Specific Expression Analysis (PSEA) to identify cell-type-specific DEGs.
  • Functional enrichment analysis (FEA) of Gene Ontology Biological Processes (GOBPs) for identified DEGs.

Main Results:

  • Identified 5,055 DEGs in APP/PS1, 1,073 in 3xTg, and 162 in hAß-KI mice, with significant overlap between fAD models.
  • fAD models exhibited higher DEG counts in neurons, oligodendrocytes, and microglia, while hAß-KI showed the highest counts in oligodendrocytes.
  • Neurons consistently showed enriched GOBPs across all models; microglia were enriched in APP/PS1, and astrocytes in 3xTg and hAß-KI models.

Conclusions:

  • fAD models displayed greater transcriptional alterations compared to the LOAD model, potentially due to more aggressive pathology.
  • Neurons are consistently affected across all AD models, underscoring their vulnerability in Alzheimer's disease.
  • The distinct transcriptional and biological signatures suggest each mouse model is suitable for studying specific aspects of AD.