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@ARTICLE{Gnrich:285478,
      author       = {Gnörich, Johannes and Kusche-Palenga, Julia and Palleis,
                      Carla and Neubauer, Antonia and Frontzkowski, Lukas and
                      Jäck, Alexander and Kling, Agnes and Bauer, Theresa and
                      Eyob, Hannah and Probst, Katharina and Roemer-Cassiano,
                      Sebastian N and Bernhardt, Alexander M and Katzdobler,
                      Sabrina and Marth, Lena and Zaganjori, Mirlind and Hopfner,
                      Franziska and Zwergal, Andreas and Häckert, Jan and
                      Rullmann, Michael and Sabri, Osama and Barthel, Henryk and
                      Stöcklein, Sophia and Werner, Rudolf A and Simons, Mikael
                      and Levin, Johannes and Herms, Jochen and Franzmeier,
                      Nicolai and Höglinger, Günter U and Brendel, Matthias},
      collaboration = {Tauopathies, German Imaging Initiative for},
      title        = {{L}ongitudinal monitoring of tau aggregation in progressive
                      supranuclear palsy with [18{F}]{PI}-2620 {PET}.},
      journal      = {Alzheimer's and dementia},
      volume       = {22},
      number       = {2},
      issn         = {1552-5260},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {DZNE-2026-00255},
      pages        = {e71195},
      year         = {2026},
      abstract     = {Progressive supranuclear palsy (PSP), a 4-repeat tauopathy,
                      can be visualized using [18F]PI-2620 tau positron emission
                      tomography (PET). However, the value of sequential
                      [18F]PI-2620 imaging for tracking tau accumulation during
                      the disease course has not yet been
                      investigated.Twenty-three PSP patients underwent two
                      [18F]PI-2620 PET scans (interval: 21.4 ± 4.3 months) and
                      were compared to cross-sectional data from 25 healthy
                      controls. Regional volume of distribution ratio values were
                      analyzed for longitudinal tau changes, clinical
                      correlations, and network-based propagation. Post mortem
                      analyses examined neuronal density and AT8 tau
                      pathology.Subcortical tau PET signals increased, strongest
                      in the globus pallidus internus (P < 0.0001). Patients with
                      low baseline tau showed the largest increases. Despite
                      clinical worsening (Progressive Supranuclear Palsy Rating
                      Scale $+48\%),$ tau PET change did not correlate with
                      symptom progression. Tau accumulation followed functional
                      connectivity (R = 0.34, P < 0.0001). Post mortem data linked
                      elevated tau PET to higher AT8 burden despite neuronal
                      loss.[18F]PI-2620 PET enables monitoring of tau progression
                      in PSP, indicating network-based tau propagation with
                      saturation in advanced stages.},
      keywords     = {Humans / Supranuclear Palsy, Progressive: diagnostic
                      imaging / Supranuclear Palsy, Progressive: metabolism /
                      Supranuclear Palsy, Progressive: pathology /
                      Positron-Emission Tomography / tau Proteins: metabolism /
                      Male / Female / Aged / Longitudinal Studies / Middle Aged /
                      Disease Progression / Brain: diagnostic imaging / Brain:
                      metabolism / Brain: pathology / Cross-Sectional Studies /
                      Fluorine Radioisotopes / Pyridines / 4‐repeat tauopathies
                      (Other) / disease monitoring (Other) / progressive
                      supranuclear palsy (Other) / tau positron emission
                      tomography (Other) / tau spreading (Other) / tau Proteins
                      (NLM Chemicals) / Fluorine Radioisotopes (NLM Chemicals) /
                      PI-2620 (NLM Chemicals) / Pyridines (NLM Chemicals)},
      cin          = {AG Haass / Clinical Research (Munich) / AG Herms / AG
                      Simons / AG Levin},
      ddc          = {610},
      cid          = {I:(DE-2719)1110007 / I:(DE-2719)1111015 /
                      I:(DE-2719)1110001 / I:(DE-2719)1110008 /
                      I:(DE-2719)1111016},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
                      Health Care Research (POF4-353) / 351 - Brain Function
                      (POF4-351)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353 /
                      G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41736364},
      pmc          = {pmc:PMC12932912},
      doi          = {10.1002/alz.71195},
      url          = {https://pub.dzne.de/record/285478},
}