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Dried Blood Spot Collection of Health Biomarkers to Maximize Participation in Population Studies
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Biomarkers.

Marina P Gonçalves1, Tevy Chan1, Arthur C Macedo1

  • 1Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Montréal, QC, Canada.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

APOEɛ4 carriers with amyloidosis show faster progression of plasma p-tau217 levels. This Alzheimer's disease biomarker change was not seen for p-tau181 or p-tau231, highlighting specific interactions in disease progression.

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Area of Science:

  • Neuroscience
  • Genetics
  • Biomarker Research

Background:

  • The apolipoprotein E ɛ4 allele (APOEɛ4) is a key genetic risk factor for Alzheimer's disease (AD).
  • APOEɛ4 carriers exhibit reduced response to amyloid-beta (Aβ) therapies and altered disease progression.
  • Plasma biomarkers offer a less invasive method for monitoring AD status and treatment response.

Purpose of the Study:

  • To investigate differences in plasma phosphorylated tau (p-tau) levels between APOEɛ4 carriers and non-carriers.
  • To examine these differences in relation to the presence or absence of cerebral amyloidosis.
  • To assess the longitudinal progression of plasma p-tau biomarkers in the context of APOEɛ4 status and amyloid positivity.

Main Methods:

  • Utilized data from the Translational Biomarkers in Aging and Dementia (TRIAD) cohort.
  • Assessed cerebral amyloid-beta and tau tangles using PET imaging.
  • Quantified plasma p-tau181, p-tau217, and p-tau231 using commercial and in-house assays.
  • Classified participants by APOEɛ4 carrier status and amyloid positivity (PET or CSF Aβ42/40 ratio).
  • Employed cross-sectional and longitudinal statistical analyses to compare biomarker levels and progression rates.

Main Results:

  • No significant baseline differences in plasma p-tau181, p-tau231, or p-tau217 were found between APOEɛ4 carriers and non-carriers, irrespective of amyloid status.
  • Longitudinal analysis revealed no differences in p-tau181 or p-tau231 progression rates based on APOEɛ4 status.
  • Accelerated increases in plasma p-tau217 were observed in amyloid-positive participants, but this progression was not significantly modulated by APOEɛ4 carrier status in A+ individuals.
  • An additive interaction between APOEɛ4 carriership and Aβ status was noted for p-tau217 progression.

Conclusions:

  • Plasma p-tau217 progression is accelerated in individuals with amyloidosis, with an additive effect from APOEɛ4 carriership.
  • APOEɛ4 status did not influence the progression rates of plasma p-tau181 or p-tau231 in the presence of amyloidosis.
  • Further research is necessary to fully elucidate the complex interplay between APOEɛ4, amyloid status, and the progression of AD biomarkers.