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

Kao Lee Yang1, Alexandra H DiFilippo2, Yazan Hammad1

  • 1Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 26, 2025
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Summary
This summary is machine-generated.

Plasma phosphorylated tau (pTau217) levels correlate with synaptic density in the entorhinal cortex, suggesting a potential early compensatory response in Alzheimer's disease (AD). Further research will explore this relationship over time.

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Area of Science:

  • Neuroscience
  • Biomarker Research
  • Alzheimer's Disease Research

Background:

  • Alzheimer's disease (AD) involves tau and amyloid pathology in synapses, potentially causing synaptic loss.
  • Plasma phosphorylated tau at 217 (pTau217) is a neuron-derived biomarker for AD pathology.
  • Understanding the link between pTau217 and synaptic changes is crucial for early AD detection and intervention.

Purpose of the Study:

  • To investigate the relationship between plasma pTau217 levels and synaptic density in medial-temporal brain regions.
  • To determine if plasma pTau217 is associated with synaptic density and cognitive impairment in individuals at risk for AD.

Main Methods:

  • Analysis of plasma pTau217 levels and [C-11]UCB-J PET scans in 50 participants.
  • Quantification of synaptic density using Logan Graphical Analysis and identification of regions of interest (ROIs).
  • Multiple regression analysis to assess associations between plasma pTau217, cognitive status, synaptic density, and amyloid positivity, controlling for age.

Main Results:

  • Higher plasma pTau217 levels were associated with higher synaptic density in the entorhinal cortex (p=0.02).
  • Cognitive impairment correlated with lower synaptic density in the entorhinal cortex (p=0.02) and hippocampus (p<0.05).
  • Effect sizes for these associations ranged from small-to-moderate to moderate-to-large.

Conclusions:

  • The observed relationship between pTau217 and synaptic density may reflect an early compensatory mechanism in response to AD pathology.
  • Most participants were cognitively unimpaired, suggesting these findings represent an early disease stage.
  • Longitudinal studies are planned to track the progression of plasma pTau217 and synaptic density over time.