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Summary
This summary is machine-generated.

Tau pathology causes brain thinning predominantly in the sulci, especially the depths, impacting memory. This sulcal vulnerability may stem from increased tau accumulation and hippocampal connectivity.

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Area of Science:

  • Neuroimaging
  • Neurodegeneration
  • Alzheimer's Disease

Background:

  • Prior research indicates sulci are uniquely affected by aging and Alzheimer's disease (AD) pathology.
  • The specific vulnerability of sulci to tau pathology and its cognitive impact remain unclear.
  • Hypothesized unique connectivity patterns in sulcal depths warrant investigation regarding tau accumulation.

Purpose of the Study:

  • To investigate whether tau-related atrophy preferentially affects sulci and their depths.
  • To explore the relationship between tau pathology, cortical thinning, and cognitive function.
  • To examine the role of hippocampal connectivity in tau-related vulnerability.

Main Methods:

  • Utilized 3T MRI and amyloid/tau PET scans from the Alzheimer's Disease Neuroimaging Initiative (ADNI).
  • Correlated cortical thickness with neocortical tau levels using FreeSurfer's GLM pipeline.
  • Analyzed overlap between tau-thickness correlation clusters and specific regions (gyri, sulci, sulcal depths); examined vertex-wise correlations and memory prediction; assessed postmortem tau and resting-state connectivity.

Main Results:

  • Tau-thickness correlation clusters showed significantly greater overlap with sulci and sulcal depths compared to gyri.
  • Sulcal regions exhibited higher tau-related cortical thinning (t-values) than gyral regions.
  • The volume of tau-affected clusters strongly predicted memory performance; postmortem analysis confirmed higher tau in sulci, and resting-state connectivity was stronger in tau-affected regions.

Conclusions:

  • Tau-related cortical thinning predominantly occurs in sulci, particularly in the depths.
  • This sulcal vulnerability is potentially linked to increased tau accumulation in these regions.
  • Enhanced hippocampal connectivity to vulnerable sulcal regions may contribute to tau pathology and cognitive decline.