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

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Summary
This summary is machine-generated.

Autosomal Dominant Alzheimer's Disease (ADAD) individuals exhibit increased brain asymmetry, measured by the Cortical Asymmetry Index (CAI). This asymmetry correlates with disease progression and key biomarkers, suggesting CAI’s potential for early detection and monitoring.

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Area of Science:

  • Neuroimaging
  • Neurodegenerative Diseases
  • Biomarker Discovery

Background:

  • Cortical Asymmetry Index (CAI) quantifies brain asymmetry, elevated in sporadic Alzheimer's Disease (AD).
  • Autosomal Dominant Alzheimer's Disease (ADAD) presents a unique model to study early AD pathogenesis.
  • Investigating CAI in asymptomatic (AMC) and symptomatic (SMC) ADAD mutation carriers is crucial for understanding disease trajectory.

Purpose of the Study:

  • To evaluate the Cortical Asymmetry Index (CAI) in asymptomatic (AMC) and symptomatic (SMC) carriers of Autosomal Dominant Alzheimer's Disease (ADAD).
  • To assess the correlation of CAI with established AD biomarkers and disease progression.
  • To explore the potential of CAI as an early detection and monitoring tool for ADAD.

Main Methods:

  • Utilized T1-weighted MRI data from two cohorts: Clinic Barcelona (N=57) and the Dominantly Inherited Alzheimer Network (DIAN, N=565).
  • Calculated CAI using Freesurfer and an open-source pipeline; analyzed cross-sectional and longitudinal changes.
  • Correlated CAI with neurofilament-light chain (NfL) levels, age, estimated years from onset (EYO), and Mini-Mental State Examination (MMSE) scores.

Main Results:

  • CAI differentiated ADAD mutation carriers (AMC and SMC) from healthy controls (CTR) in the Clinic Barcelona cohort.
  • In the DIAN cohort, CAI distinguished symptomatic AD (SMC-AD) from CTR and AMC, and correlated with elevated NfL, reduced MMSE, and advanced EYO.
  • Longitudinal analysis revealed a significant increase in CAI over time in SMC and SMC-AD individuals.

Conclusions:

  • ADAD individuals demonstrate progressive brain asymmetry, with CAI correlating with key AD biomarkers.
  • APOE3/3 genotype showed distinct asymmetry patterns compared to other genotypes.
  • CAI's significant longitudinal increase in symptomatic carriers highlights its potential as a sensitive marker for AD progression and monitoring.