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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.

Tengfei Guo1,2,3, Yue Cai1, Jie Yang1

  • 1Shenzhen Bay Laboratory, Shenzhen, Guangdong, China.

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

Higher education, lower sTREM2, higher GFAP, and more white matter hyperintensities accelerate Alzheimer's disease tau accumulation beyond amyloid-beta. Controlling these factors is crucial for preventing tau spread.

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Area of Science:

  • Neuroscience
  • Neurology
  • Gerontology

Background:

  • Alzheimer's disease (AD) is characterized by beta-amyloid (Aβ) plaques and tau tangles.
  • Aβ plaques correlate with tau accumulation in early AD.
  • The influence of educational attainment (EA), neuroinflammation, and vascular disease on tau spread remains unclear.

Purpose of the Study:

  • To investigate how EA, neuroinflammation markers (sTREM2, GFAP), and white matter hyperintensities (WMH) affect cortical tau accumulation in AD.
  • To analyze tau PET imaging data from East Asian (GHABS) and Western (ADNI, A4) older populations.

Main Methods:

  • Analysis of tau PET imaging data from GHABS, ADNI, and A4 studies.
  • Correlation analysis of EA status, plasma sTREM2 and GFAP concentrations, and WMH with cortical tau accumulation.
  • Investigation of modulation effects on Aβ-, entorhinal tau-, and plasma p-Tau-related tau aggregation.

Main Results:

  • Higher EA was associated with stronger links between Aβ burden, entorhinal tau, plasma p-Tau217, and tau accumulation in Aβ+ individuals.
  • Higher plasma sTREM2 correlated with weaker Aβ-related tau accumulation, while higher GFAP correlated with stronger accumulation.
  • Increased WMH burden was linked to faster tau accumulation in the occipital lobe, independent of Aβ, potentially due to connectivity-related tau spread.

Conclusions:

  • Factors including education, plasma sTREM2 and GFAP levels, and WMH burden influence tau accumulation in AD, alongside Aβ pathology.
  • Controlling these non-Aβ factors is important for preventing tau aggregation in Alzheimer's disease.