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Biomarkers.

Aurélie Lebrun1,2, Yann Leprince1, Julien Lagarde2,3,4

  • 1Université Paris-Saclay, CEA, NeuroSpin, UNIACT, Gif-sur-Yvette, France.

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

White matter (WM) damage progresses in Alzheimer's disease (AD) and Limbic-predominant Age-related TDP-43 Encephalopathy (LATE) over two years. This progression is more significant in patients than in controls, highlighting WM's role in these neurodegenerative diseases.

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Area of Science:

  • Neuroimaging
  • Neurodegenerative Diseases
  • White Matter Integrity

Background:

  • Alzheimer's disease (AD) and Limbic-predominant Age-related TDP-43 Encephalopathy (LATE) are distinct neurodegenerative conditions presenting with similar memory loss.
  • Previous studies indicated white matter (WM) alterations in AD and LATE, suggesting WM damage may contribute to disease pathology.
  • This study investigates the longitudinal changes in WM integrity in early AD and LATE.

Purpose of the Study:

  • To examine the two-year progression of white matter (WM) fiber bundle alterations in early Alzheimer's disease (AD) and Limbic-predominant Age-related TDP-43 Encephalopathy (LATE).
  • To compare the rate of WM changes between AD patients, LATE patients, and healthy controls.
  • To elucidate the role of WM damage in the progression of these neurodegenerative diseases.

Main Methods:

  • Inclusion of 16 AD patients, 12 LATE patients, and 15 healthy controls, confirmed by clinical and biomarker criteria.
  • Two 3-tesla MRI scans were acquired two years apart for all participants.
  • Whole-brain and tract-based fixel-based analyses using multi-shell diffusion MRI were performed to assess WM fiber density and cross-section changes over time, controlling for age and sex.

Main Results:

  • White matter (WM) fiber bundle damage progressed in both AD and LATE patient groups over the two-year period.
  • Patients showed a more pronounced decline in WM integrity compared to controls, particularly in tracts connecting temporal, parietal, and frontal lobes (e.g., arcuate fasciculus, middle longitudinal fasciculus).
  • Specific tracts showed differential progression: AD patients had greater decline in the cingulum and inferior longitudinal fasciculus, while LATE patients showed more decline in the superior longitudinal fasciculus.

Conclusions:

  • White matter (WM) fiber bundle alterations are a progressive feature in both Alzheimer's disease (AD) and Limbic-predominant Age-related TDP-43 Encephalopathy (LATE).
  • The rate of WM deterioration is significantly higher in patients with AD and LATE compared to healthy individuals.
  • These findings underscore the critical role and progressive nature of WM damage in the pathophysiology of AD and LATE.