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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.

Christopher A Brown1, Sandhitsu R Das1, Katheryn A Q Cousins1

  • 1University of Pennsylvania, Philadelphia, PA, USA.

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

Individuals with Alzheimer's disease showing a biological-clinical mismatch, particularly those vulnerable, exhibit accelerated cognitive decline and increased alpha-synuclein co-pathology. This tau-cognitive mismatch highlights distinct neurodegenerative patterns and aids in identifying at-risk populations.

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Area of Science:

  • Neuroscience
  • Biomarkers in neurodegenerative diseases
  • Clinical staging of Alzheimer's disease

Background:

  • Revised Alzheimer's disease (AD) staging incorporates biological-clinical mismatch, categorizing individuals as vulnerable or resilient based on clinical impairment relative to biological stage.
  • This study utilized plasma p-tau217 and 18F-flortaucipir PET (T2) biomarkers to assess mismatch against global clinical severity (CDR-SB).
  • Investigated differences in brain structure, alpha-synuclein positivity, and longitudinal changes in cognition, tau accumulation, and atrophy among canonical, vulnerable, and resilient groups.

Purpose of the Study:

  • To identify biological-clinical mismatch in Alzheimer's disease using tau biomarkers (p-tau217 and Tau-MaX) and clinical severity (CDR-SB).
  • To investigate neurodegenerative differences, alpha-synuclein co-pathology, and longitudinal trajectories in canonical, vulnerable, and resilient groups.
  • To validate the tau-cognitive mismatch model in an independent dataset.

Main Methods:

  • Included amyloid-positive ADNI participants with available Tau PET or p-tau217 and CDR-SB scores.
  • Defined mismatch using linear regression between tau burden (Tau-MaX or p-tau217) and CDR-SB, categorizing participants into canonical, vulnerable, and resilient groups.
  • Analyzed medial temporal lobe (MTL) structure, brain-wide thickness, alpha-synuclein status, and longitudinal tau PET, atrophy, and cognitive trajectories, controlling for covariates. Replicated findings in the Penn ADRC dataset.

Main Results:

  • Both Tau-MaX and p-tau217 showed moderate association with CDR-SB.
  • Vulnerable individuals exhibited greater neurodegeneration in anterior MTL and temporolimbic regions and higher alpha-synuclein prevalence.
  • The vulnerable group demonstrated accelerated cognitive decline independent of tau accumulation rate and faster atrophy in MTL and temporolimbic regions. Findings were consistent across ADNI and Penn ADRC datasets.

Conclusions:

  • Tau-cognitive mismatch effectively identifies vulnerable individuals with distinct neurodegeneration patterns and alpha-synuclein co-pathology, overlapping with Limbic-predominant Age-Related TDP-43 Encephalopathy (LATE).
  • Plasma-based tau biomarkers successfully identified similar vulnerable individuals in an independent cohort, suggesting clinical utility.
  • This approach refines understanding of AD progression heterogeneity and identifies individuals requiring targeted interventions.