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@ARTICLE{Zhu:283122,
      author       = {Zhu, Zeyu and Steward, Anna and Dehsarvi, Amir and
                      Roemer-Cassiano, Sebastian N. and Dewenter, Anna and Biel,
                      Davina and Hirsch, Fabian and Frontzkowski, Lukas and
                      Pescoller, Julia and Klonowski, Madleen and Gnoerich,
                      Johannes and Pontecorvo, Michael J. and Shcherbinin, Sergey
                      and Schöll, Michael and Buckley, Rachel and Ossenkoppele,
                      Rik and Xie, Fang and Guo, Tengfei and Höglinger, Günter
                      and Brendel, Matthias and Franzmeier, Nicolai},
      title        = {{D}efining patient‐centered amyloid {PET} thresholds for
                      the onset of tauopathy in {A}lzheimer's disease},
      journal      = {Alzheimer's and dementia},
      volume       = {22},
      number       = {1},
      issn         = {1552-5260},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {DZNE-2026-00018},
      pages        = {e71064},
      year         = {2026},
      abstract     = {Amyloid-induced tauopathy drives clinical decline in
                      Alzheimer's disease (AD). Because age and sex shape tau
                      trajectories, defining patient-centered amyloid thresholds
                      for tauopathy onset could facilitate pre-tauopathy AD
                      identification and aid treatment decisions and prognosis.By
                      including two samples (Alzheimer's Disease Neuroimaging
                      Initiative [ADNI, n = 301]; and 18F-AV-1451-A05 [A05, n =
                      143]), we explored whether age and sex affect tauopathy
                      transition and determined patient-centered amyloid positron
                      emission tomography (PET) thresholds that mark tauopathy
                      onset.We found a consistent amyloid PET × age interaction
                      on global tau PET increase in men (ADNI/A05: p =
                      0.0078/0.018), with younger men showing faster
                      amyloid-associated tau accumulation. We then established
                      patient-centered, amyloid PET-inferred tauopathy transition
                      cut-offs. Women reached this transition at lower amyloid PET
                      levels, and these cutoffs predicted both earlier onset and
                      accelerated cognitive decline (p < 0.001).This study
                      highlights the effect of age and sex on the
                      amyloid-to-tauopathy transition, establishes
                      patient-centered amyloid PET thresholds for tauopathy onset,
                      and links these thresholds to accelerated cognitive
                      decline.Younger age is related to faster amyloid-related tau
                      accumulation in men. We defined a series of amyloid positron
                      emission tomography (PET) thresholds to enable
                      patient-centered inference of amyloid-related tauopathy.
                      Crossing the amyloid PET-defined tauopathy phase is
                      associated with more progressive tau deposition and
                      cognitive decline.},
      keywords     = {Humans / Positron-Emission Tomography / Male / Alzheimer
                      Disease: diagnostic imaging / Alzheimer Disease: metabolism
                      / Female / Tauopathies: diagnostic imaging / Tauopathies:
                      metabolism / Aged / tau Proteins: metabolism / Aged, 80 and
                      over / Amyloid: metabolism / Sex Factors / Age Factors /
                      Brain: diagnostic imaging / Brain: metabolism / Carbolines},
      cin          = {Clinical Research (Munich) / AG Haass},
      ddc          = {610},
      cid          = {I:(DE-2719)1111015 / I:(DE-2719)1110007},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41485137},
      doi          = {10.1002/alz.71064},
      url          = {https://pub.dzne.de/record/283122},
}