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Blood Studies for Cardiovascular System I: Cardiac Biomarkers01:20

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Cardiac biomarkers are enzymes, proteins, and hormones released into the blood when cardiac cells are injured. They are powerful tools for triaging.
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Dried Blood Spot Collection of Health Biomarkers to Maximize Participation in Population Studies
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Biomarkers.

Wiesje Pelkmans1,2, Mahnaz Shekari1,3,4, Armand González Escalante1,4

  • 1Barcelonaβeta Brain Research Center (BBRC), Pasqual Maragall Foundation, Barcelona, Spain.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
PubMed
Summary
This summary is machine-generated.

Soluble tau phosphorylated at threonine 231 (p-tau231) in early Alzheimer's disease may activate microglial TREM2, a response that appears to slow amyloid-beta (Aβ) accumulation. This suggests enhancing microglial function could be a therapeutic strategy for preclinical AD.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Soluble tau phosphorylated at threonine 231 (p-tau231) is elevated in preclinical Alzheimer's disease (AD), preceding amyloid-beta (Aβ) PET positivity.
  • The mechanisms linking early tau phosphorylation to subsequent Aβ accumulation are unclear, though microglial reactivity is implicated in Aβ dynamics.
  • Microglia play a dual role in Aβ metabolism, potentially clearing Aβ or promoting its accumulation through neuroinflammation.

Purpose of the Study:

  • To investigate the association between cerebrospinal fluid (CSF) p-tau231 levels and longitudinal Aβ accumulation in cognitively unimpaired individuals.
  • To examine the role of TREM2-mediated microglial reactivity, assessed by CSF sTREM2 levels, in the relationship between p-tau231 and Aβ accumulation.
  • To determine if microglial reactivity mediates the link between early tau phosphorylation and subsequent Aβ deposition.

Main Methods:

  • Studied 187 cognitively unimpaired individuals from the ALFA+ cohort with repeated Aβ-PET imaging.
  • Utilized linear regression models and mediation analysis to assess associations between CSF p-tau231, longitudinal Aβ accumulation (centiloid change), and CSF sTREM2.
  • Adjusted models for baseline Aβ levels, age, APOE-ε4 status, and sex.

Main Results:

  • Higher CSF p-tau231 levels were significantly associated with faster Aβ-PET accumulation (p < 0.01).
  • Elevated p-tau231 correlated with increased CSF sTREM2 levels (p < 0.001), indicating heightened TREM2-mediated microglial reactivity.
  • Higher sTREM2 levels were linked to reduced Aβ accumulation rates (p < 0.01), mediating 27% of the p-tau231 effect on Aβ-PET.

Conclusions:

  • Early-stage soluble tau phosphorylation may enhance TREM2-mediated microglial reactivity.
  • This microglial response appears to be a protective mechanism that slows fibrillar Aβ accumulation in preclinical AD.
  • Therapeutic strategies aimed at enhancing microglial function in preclinical AD could potentially delay or prevent Aβ buildup.