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Biomarkers.

Briar Nowling1, Hamsanandini Radhakrishnan2, Christopher A Olm2

  • 1Frontotemporal Degeneration Center, University of Pennsylvania, Philadelphia, PA, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
PubMed
Summary
This summary is machine-generated.

Non-amnestic Alzheimer's disease (AD) shows reduced white matter (WM) connectivity compared to amnestic AD. This degeneration correlates with tau buildup and brain atrophy, linking WM changes to tau progression in AD.

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Area of Science:

  • Neuroscience
  • Neuropathology
  • Radiology

Background:

  • Non-amnestic Alzheimer's disease (AD) exhibits greater white matter (WM) degeneration than amnestic AD.
  • Understanding the relationship between WM changes and AD pathophysiology is crucial for explaining earlier onset and atypical tau distribution in non-amnestic AD.
  • This study hypothesizes that WM degeneration correlates with tau burden and grey matter atrophy in fiber tract endpoints, linking WM changes to tau progression.

Purpose of the Study:

  • To investigate the relationship between white matter (WM) degeneration, tau burden, and grey matter atrophy in different Alzheimer's disease (AD) variants.
  • To compare WM connectivity (using generalized fractional anisotropy - GFA and nodal degree) between amnestic and non-amnestic AD.
  • To explore the association between tau deposition, regional atrophy, and WM integrity in individuals with AD.

Main Methods:

  • Included 46 participants with normal cognition or AD, categorized into amnestic and various non-amnestic syndromes.
  • Assessed tau burden using flortaucipir PET scans and WM integrity using diffusion MRI-derived GFA and nodal degree.
  • Employed linear mixed effects models to analyze differences in GFA and nodal degree and tested associations between GFA and tau burden (SUVR) in tract endpoints.

Main Results:

  • Non-amnestic AD showed significantly lower nodal degree, indicating sparser connectivity, though GFA did not differ between groups.
  • Tau burden (SUVR) increased with higher atrophy tertiles across AD variants (p < 0.0001).
  • WM integrity (GFA) was reduced in tracts connecting to areas of higher atrophy, and higher tau SUVR in cortical endpoints was associated with lower tractwise GFA (p < 0.0001).

Conclusions:

  • Replicated findings of reduced WM connectivity in non-amnestic compared to amnestic AD.
  • Demonstrated that WM integrity is associated with tau burden and atrophy in the endpoints of fiber tracts.
  • Confirmed consistency of results across diverse non-amnestic syndromes, linking WM degeneration to core AD pathologies.