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Basic Science and Pathogenesis.

Hannah M Klinger1, Vaibhav A Janve2, Mabel Seto1,3

  • 1Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.

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Summary
This summary is machine-generated.

Whole blood gene expression in unimpaired older adults showed associations with cognitive decline, particularly when interacting with Alzheimer's disease biomarkers like Aβ-PET and p-tau217.

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Area of Science:

  • Neuroscience
  • Genomics
  • Biomarkers

Background:

  • Bulk brain tissue studies link gene expression to Alzheimer's disease (AD) and cognitive decline.
  • Previous findings focused on older adults and end-of-life changes.
  • Identifying early AD biological pathways in accessible samples like blood is crucial.

Purpose of the Study:

  • To identify whole blood transcriptomic signals associated with cognitive decline in clinically unimpaired older adults.
  • To explore relationships between gene expression and in vivo AD phenotypes (Aβ-PET, p-tau217).
  • To elucidate early biological pathways implicated in Alzheimer's disease.

Main Methods:

  • Analyzed whole blood gene expression data from 1,737 participants in the A4 and LEARN studies.
  • Used linear mixed-effects models to assess associations between gene expression and longitudinal cognitive performance (PACC).
  • Investigated interactions between gene expression, sex, APOEε4 status, Aβ-PET burden, and p-tau217 levels, with FDR correction.

Main Results:

  • No single gene transcript directly correlated with cognitive decline after FDR correction.
  • 167 genes showed associations with cognition when interacting with biomarkers.
  • Specific genes (e.g., ETF1P2, ZSCAN2) were linked to faster cognitive decline in individuals with high Aβ-PET burden, with some interactions involving sex and APOEε4.

Conclusions:

  • Whole blood transcriptomic signals are associated with cognitive decline primarily through interactions with Alzheimer's disease biomarkers (Aβ-PET, p-tau217) and sex.
  • These findings highlight the potential of blood-based gene expression for understanding early AD pathogenesis.
  • Further research, including enrichment analysis and external validation, is needed to fully elucidate the involved biological pathways.