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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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Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
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Dried Blood Spot Collection of Health Biomarkers to Maximize Participation in Population Studies
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Biomarkers.

Ting Qiu1,2,3,4, Zhen-Qi Liu5,6, Jonathan Gallego Rudolf5,7,8

  • 1Integrated Program in Neurosciences, McGill University, Montréal, QC, Canada.

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

Alzheimer's disease (AD) brain changes, including cortical thickness and diffusivity, begin years before symptoms. These structural alterations follow nonlinear patterns in response to amyloid-beta (Aβ) pathology.

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Area of Science:

  • Neuroimaging
  • Alzheimer's Disease Research
  • Brain Structure Analysis

Background:

  • Alzheimer's disease (AD) involves amyloid-beta (Aβ) and tau pathology, typically linked to grey matter loss.
  • Preclinical AD may show increased cortical thickness (CT), contrasting with later-stage reductions.
  • Longitudinal data is crucial for understanding early structural changes in AD progression.

Purpose of the Study:

  • To investigate the association between Aβ and tau pathology and brain structure (CT, mean diffusivity [MDT], hippocampal volume) over 10 years.
  • To determine the longitudinal trajectories of structural brain changes relative to Aβ positivity.
  • To explore changes across preclinical and prodromal stages of AD.

Main Methods:

  • Partial least square analyses (PLS) were used to identify pathological-structural associations in Aβ-negative and Aβ-positive groups.
  • Cross-sectional and longitudinal associations between AD pathology and structural measures were assessed.
  • Time from Aβ positivity onset was estimated to track structural changes over time.

Main Results:

  • Higher Aβ deposition correlated with decreased MDT and increased CT in Aβ-negative individuals.
  • Aβ-positive individuals showed opposite associations (increased MDT, decreased CT).
  • MDT followed a U-shaped pattern and CT an inverse U-shaped pattern with Aβ pathology, appearing years before Aβ positivity.

Conclusions:

  • Brain structural changes in response to Aβ pathology commence decades before clinical symptoms.
  • These changes exhibit highly nonlinear trajectories, potentially involving neuroinflammation or brain swelling.
  • Understanding these early nonlinear changes is key for preclinical AD intervention.