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Drug Development.

Tammie L S Benzinger1, Arnaud Charil2, Brian A Gordon3

  • 1Washington University School of Medicine in St. Louis, St. Louis, MO, USA.

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|December 25, 2025
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Dominantly Inherited Alzheimer Disease (DIAD) patients show distinct tau PET and MRI differences between symptomatic and asymptomatic groups. Symptomatic individuals exhibit higher tau accumulation and brain atrophy, particularly in the parietal cortex.

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Area of Science:

  • Neurology
  • Neuroimaging
  • Alzheimer's Disease Research

Background:

  • The DIAN-TU-001 trial investigates anti-tau antibody etalanetug (E2814) in Dominantly Inherited Alzheimer Disease (DIAD).
  • This study arm of the Tau NexGen platform is a placebo-controlled, double-blind Phase II/III trial.
  • It evaluates E2814, alone or with lecanemab, focusing on biomarkers, efficacy, safety, and tolerability.

Purpose of the Study:

  • To report baseline imaging characteristics of participants in the DIAN-TU-001 trial.
  • To compare imaging biomarkers between symptomatic and asymptomatic DIAD individuals.
  • To establish a baseline for evaluating the therapeutic effects of anti-tau antibodies.

Main Methods:

  • Amyloid 11C-PiB PET SUVr converted to Centiloids.
  • 18F-MK6240 Tau SUVr and volumetric MRI (vMRI) calculated for Braak stage and composite regions.
  • Comparison of imaging metrics between symptomatic and asymptomatic DIAD participants.

Main Results:

  • Symptomatic DIAD subjects have higher baseline amyloid levels (99.86 CL) than asymptomatic carriers (30.62 CL).
  • Symptomatic individuals show increased tau PET SUVr values (1.94-3.00) and greater brain atrophy across regions, especially the parietal cortex.
  • Tau accumulation patterns in symptomatic DIAD differ from sporadic AD, with early parietal involvement.

Conclusions:

  • Baseline imaging reveals significant spatial tau PET and vMRI differences between symptomatic and asymptomatic DIAD subjects.
  • Amyloid levels correlate with disease stage in DIAD.
  • Symptomatic DIAD patients present with elevated tau and atrophy, particularly in the parietal cortex, supporting distinct pathology compared to sporadic AD.