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| 001 | 283122 | ||
| 005 | 20260105130452.0 | ||
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| 037 | _ | _ | |a DZNE-2026-00018 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Zhu, Zeyu |b 0 |
| 245 | _ | _ | |a Defining patient‐centered amyloid PET thresholds for the onset of tauopathy in Alzheimer's disease |
| 260 | _ | _ | |a Hoboken, NJ |c 2026 |b Wiley |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 520 | _ | _ | |a 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. |
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| 536 | _ | _ | |a 352 - Disease Mechanisms (POF4-352) |0 G:(DE-HGF)POF4-352 |c POF4-352 |f POF IV |x 1 |
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| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a Positron-Emission Tomography |2 MeSH |
| 650 | _ | 2 | |a Male |2 MeSH |
| 650 | _ | 2 | |a Alzheimer Disease: diagnostic imaging |2 MeSH |
| 650 | _ | 2 | |a Alzheimer Disease: metabolism |2 MeSH |
| 650 | _ | 2 | |a Female |2 MeSH |
| 650 | _ | 2 | |a Tauopathies: diagnostic imaging |2 MeSH |
| 650 | _ | 2 | |a Tauopathies: metabolism |2 MeSH |
| 650 | _ | 2 | |a Aged |2 MeSH |
| 650 | _ | 2 | |a tau Proteins: metabolism |2 MeSH |
| 650 | _ | 2 | |a Aged, 80 and over |2 MeSH |
| 650 | _ | 2 | |a Amyloid: metabolism |2 MeSH |
| 650 | _ | 2 | |a Sex Factors |2 MeSH |
| 650 | _ | 2 | |a Age Factors |2 MeSH |
| 650 | _ | 2 | |a Brain: diagnostic imaging |2 MeSH |
| 650 | _ | 2 | |a Brain: metabolism |2 MeSH |
| 650 | _ | 2 | |a Carbolines |2 MeSH |
| 700 | 1 | _ | |a Steward, Anna |b 1 |
| 700 | 1 | _ | |a Dehsarvi, Amir |b 2 |
| 700 | 1 | _ | |a Roemer-Cassiano, Sebastian N. |b 3 |
| 700 | 1 | _ | |a Dewenter, Anna |b 4 |
| 700 | 1 | _ | |a Biel, Davina |b 5 |
| 700 | 1 | _ | |a Hirsch, Fabian |b 6 |
| 700 | 1 | _ | |a Frontzkowski, Lukas |b 7 |
| 700 | 1 | _ | |a Pescoller, Julia |b 8 |
| 700 | 1 | _ | |a Klonowski, Madleen |b 9 |
| 700 | 1 | _ | |a Gnoerich, Johannes |0 P:(DE-2719)9001652 |b 10 |u dzne |
| 700 | 1 | _ | |a Pontecorvo, Michael J. |b 11 |
| 700 | 1 | _ | |a Shcherbinin, Sergey |b 12 |
| 700 | 1 | _ | |a Schöll, Michael |b 13 |
| 700 | 1 | _ | |a Buckley, Rachel |b 14 |
| 700 | 1 | _ | |a Ossenkoppele, Rik |b 15 |
| 700 | 1 | _ | |a Xie, Fang |b 16 |
| 700 | 1 | _ | |a Guo, Tengfei |b 17 |
| 700 | 1 | _ | |a Höglinger, Günter |0 P:(DE-2719)2811373 |b 18 |u dzne |
| 700 | 1 | _ | |a Brendel, Matthias |0 P:(DE-2719)9001539 |b 19 |u dzne |
| 700 | 1 | _ | |a Franzmeier, Nicolai |0 0000-0001-9736-2283 |b 20 |
| 773 | _ | _ | |a 10.1002/alz.71064 |g Vol. 22, no. 1, p. e71064 |0 PERI:(DE-600)2201940-6 |n 1 |p e71064 |t Alzheimer's and dementia |v 22 |y 2026 |x 1552-5260 |
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