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

Agnès Pérez-Millan1,2, Beatriz Bosch-Capdevila1, Sergi Borrego-Écija1

  • 1Alzheimer's disease and other cognitive disorders Group. Service of Neurology, Hospital Clínic de Barcelona. Fundació Recerca Clínic Barcelona-IDIBAPS, Barcelona, Spain.

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

Autosomal Dominant Alzheimer's Disease (ADAD) mutation carriers show increased brain asymmetry (CAI) that correlates with disease biomarkers. This brain asymmetry marker (CAI) significantly increases over time in symptomatic individuals, indicating its potential for early detection and monitoring.

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Area of Science:

  • Neuroscience
  • Neurology
  • Medical Imaging

Background:

  • Cortical Asymmetry Index (CAI) quantifies brain asymmetry, with higher levels observed in sporadic Alzheimer's Disease (AD).
  • This study investigates CAI in asymptomatic (AMC) and symptomatic (SMC) mutation carriers of Autosomal Dominant Alzheimer's Disease (ADAD).

Purpose of the Study:

  • To evaluate the Cortical Asymmetry Index (CAI) as a potential biomarker for Autosomal Dominant Alzheimer's Disease (ADAD).
  • To assess CAI in asymptomatic (AMC) and symptomatic (SMC) ADAD mutation carriers and its correlation with disease progression and biomarkers.

Main Methods:

  • Utilized T1-weighted MRI data from two cohorts: Clinic Barcelona (N=56) and DIAN-OBS (N=464).
  • Calculated CAI using Freesurfer and an open-source pipeline; analyzed cross-sectional and longitudinal data, including cerebrospinal fluid (CSF) and plasma neurofilament-light chain (NfL) levels.
  • Assessed correlations between CAI, age, estimated years from onset (EYO), Mini-Mental State Examination (MMSE) scores, and NfL levels; examined APOE genotype effects.

Main Results:

  • CAI differentiated ADAD mutation carriers (AMC and SMC) from healthy controls (CTR) and identified SMC-AD from CTR and AMC.
  • Elevated CAI in carriers and SMC correlated with higher plasma NfL, advanced EYO, and lower MMSE scores.
  • Longitudinally, CAI significantly increased over time in SMC and SMC-AD individuals within the DIAN cohort.

Conclusions:

  • ADAD individuals exhibit increased brain asymmetry that progresses with the disease and correlates with key AD biomarkers.
  • CAI shows significant longitudinal increases in symptomatic ADAD individuals, highlighting its potential for disease monitoring.
  • CAI is a promising tool for early detection and tracking of AD progression in Autosomal Dominant Alzheimer's Disease.