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Basic Science and Pathogenesis.

Mabel Seto1, Hannah M Klinger1, Vaibhav A Janve2

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Summary
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Plasma p-tau217 is an early Alzheimer's disease (AD) marker. X-linked gene expression, moderated by amyloid-beta (Aβ) burden and sex, influences p-tau217 levels in cognitively normal older adults.

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Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • Plasma p-tau217 is a sensitive, early Alzheimer's disease (AD) biomarker, correlating with Aβ-PET burden and cognitive decline.
  • Previous research on X-linked genes in AD used postmortem tissue, limiting relevance to early disease stages.
  • Understanding X-linked gene expression in early AD is crucial for developing timely interventions.

Purpose of the Study:

  • To investigate associations between whole blood X-linked gene expression and plasma p-tau217 levels.
  • To explore how these associations are modified by amyloid-beta (Aβ) burden, sex, and APOEε4 status.
  • To identify potential X-linked genetic risk or protective factors in early AD.

Main Methods:

  • Analysis of whole blood RNA sequencing, plasma p-tau217, and Aβ-PET data from 724 cognitively unimpaired older adults.
  • Linear regression models were used to assess direct gene associations and interactions with Aβ, sex, and APOEε4.
  • Results were FDR-corrected for over 20,000 autosomal and X-linked genes.

Main Results:

  • No direct associations were found between X-linked genes and p-tau217 levels.
  • 119 X-linked genes showed moderation by Aβ burden, and 27 by the Aβ*sex interaction, on p-tau217 levels.
  • Four genes (FAM156B, KDM6A, WWC3, MID1IP1) previously implicated in AD showed complex associations with p-tau217, dependent on Aβ burden and sex.

Conclusions:

  • X-linked gene expression associations with plasma p-tau217 in early AD are significantly moderated by Aβ burden and sex.
  • This study identified potential protective (e.g., FAM156B, WWC3 in females) and risk (e.g., KDM6A, WWC3 in males, MID1IP1) X-linked genes.
  • Findings underscore the importance of considering sex chromosomes and sex-specific effects in AD research.