% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Brendel:889144,
      author       = {Brendel, Matthias and Barthel, Henryk and van Eimeren,
                      Thilo and Marek, Ken and Beyer, Leonie and Song, Mengmeng
                      and Palleis, Carla and Gehmeyr, Mona and Fietzek, Urban and
                      Respondek, Gesine and Sauerbeck, Julia and Nitschmann,
                      Alexander and Zach, Christian and Hammes, Jochen and Barbe,
                      Michael T. and Onur, Oezguer and Jessen, Frank and Saur,
                      Dorothee and Schroeter, Matthias L. and Rumpf, Jost-Julian
                      and Rullmann, Michael and Schildan, Andreas and Patt,
                      Marianne and Neumaier, Bernd and Barret, Olivier and
                      Madonia, Jennifer and Russell, David S. and Stephens, Andrew
                      and Roeber, Sigrun and Herms, Jochen and Bötzel, Kai and
                      Classen, Joseph and Bartenstein, Peter and Villemagne,
                      Victor and Levin, Johannes and Höglinger, Günter U. and
                      Drzezga, Alexander and Seibyl, John and Sabri, Osama},
      title        = {{A}ssessment of 18 {F}-{PI}-2620 as a {B}iomarker in
                      {P}rogressive {S}upranuclear {P}alsy},
      journal      = {JAMA neurology},
      volume       = {77},
      number       = {11},
      issn         = {2168-6149},
      address      = {Chicago, Ill.},
      publisher    = {American Medical Association},
      reportid     = {FZJ-2021-00069},
      pages        = {1408 -},
      year         = {2020},
      abstract     = {Importance: Progressive supranuclear palsy (PSP) is a
                      4-repeat tauopathy. Region-specific tau aggregates establish
                      the neuropathologic diagnosis of definite PSP post mortem.
                      Future interventional trials against tau in PSP would
                      strongly benefit from biomarkers that support
                      diagnosis.Objective: To investigate the potential of the
                      novel tau radiotracer 18F-PI-2620 as a biomarker in patients
                      with clinically diagnosed PSP.Design, setting, and
                      participants: In this cross-sectional study, participants
                      underwent dynamic 18F-PI-2620 positron emission tomography
                      (PET) from 0 to 60 minutes after injection at 5 different
                      centers (3 in Germany, 1 in the US, and 1 in Australia).
                      Patients with PSP (including those with Richardson syndrome
                      [RS]) according to Movement Disorder Society PSP criteria
                      were examined together with healthy controls and controls
                      with disease. Four additionally referred individuals with
                      PSP-RS and 2 with PSP-non-RS were excluded from final data
                      analysis owing to incomplete dynamic PET scans. Data were
                      collected from December 2016 to October 2019 and were
                      analyzed from December 2018 to December 2019.Main outcomes
                      and measures: Postmortem autoradiography was performed in
                      independent PSP-RS and healthy control samples. By in vivo
                      PET imaging, 18F-PI-2620 distribution volume ratios were
                      obtained in globus pallidus internus and externus, putamen,
                      subthalamic nucleus, substantia nigra, dorsal midbrain,
                      dentate nucleus, dorsolateral, and medial prefrontal cortex.
                      PET data were compared between patients with PSP and control
                      groups and were corrected for center, age, and sex.Results:
                      Of 60 patients with PSP, 40 $(66.7\%)$ had RS (22 men
                      $[55.0\%];$ mean [SD] age, 71 [6] years; mean [SD] PSP
                      rating scale score, 38 [15]; score range, 13-71) and 20
                      $(33.3\%)$ had PSP-non-RS (11 men $[55.0\%];$ mean [SD] age,
                      71 [9] years; mean [SD] PSP rating scale score, 24 [11];
                      score range, 11-41). Ten healthy controls (2 men; mean [SD]
                      age, 67 [7] years) and 20 controls with disease (of 10
                      $[50.0\%]$ with Parkinson disease and multiple system
                      atrophy, 7 were men; mean [SD] age, 61 [8] years; of 10
                      $[50.0\%]$ with Alzheimer disease, 5 were men; mean [SD]
                      age, 69 [10] years). Postmortem autoradiography showed
                      blockable 18F-PI-2620 binding in patients with PSP and no
                      binding in healthy controls. The in vivo findings from the
                      first large-scale observational study in PSP with
                      18F-PI-2620 indicated significant elevation of tracer
                      binding in PSP target regions with strongest differences in
                      PSP vs control groups in the globus pallidus internus (mean
                      [SD] distribution volume ratios: PSP-RS, 1.21 [0.10];
                      PSP-non-RS, 1.12 [0.11]; healthy controls, 1.00 [0.08];
                      Parkinson disease/multiple system atrophy, 1.03 [0.05];
                      Alzheimer disease, 1.08 [0.06]). Sensitivity and specificity
                      for detection of PSP-RS vs any control group were $85\%$ and
                      $77\%,$ respectively, when using classification by at least
                      1 positive target region.Conclusions and relevance: This
                      multicenter evaluation indicates a value of 18F-PI-2620 to
                      differentiate suspected patients with PSP, potentially
                      facilitating more reliable diagnosis of PSP.},
      cin          = {INM-2 / INM-5},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-2-20090406 / I:(DE-Juel1)INM-5-20090406},
      pnm          = {572 - (Dys-)function and Plasticity (POF3-572) / 573 -
                      Neuroimaging (POF3-573)},
      pid          = {G:(DE-HGF)POF3-572 / G:(DE-HGF)POF3-573},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {33165511},
      UT           = {WOS:000593760500013},
      doi          = {10.1001/jamaneurol.2020.2526},
      url          = {https://juser.fz-juelich.de/record/889144},
}