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@ARTICLE{Kovacs:151075,
      author       = {Kovacs, Gabor G. and Irwin, David J. and Jecmenica Lukic,
                      Milica and Arzberger, Thomas and Respondek, Gesine and Lee,
                      Edward B. and Coughlin, David and Giese, Armin and Grossman,
                      Murray and Kurz, Carolin and McMillan, Corey T. and Gelpi,
                      Ellen and Compta, Yaroslau and van Swieten, John C. and
                      Laat, Laura Donker and Troakes, Claire and Al-Sarraj, Safa
                      and Robinson, John L. and Roeber, Sigrun and Xie, Sharon X.
                      and Lee, Virginia M.- Y. and Trojanowski, John Q. and
                      Höglinger, Günter U.},
      title        = {{D}istribution patterns of tau pathology in progressive
                      supranuclear palsy},
      journal      = {Acta neuropathologica},
      volume       = {140},
      number       = {2},
      issn         = {0001-6322},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DZNE-2020-01060},
      pages        = {99-119},
      year         = {2020},
      abstract     = {Progressive supranuclear palsy (PSP) is a 4R-tauopathy
                      predominated by subcortical pathology in neurons,
                      astrocytes, and oligodendroglia associated with various
                      clinical phenotypes. In the present international study, we
                      addressed the question of whether or not sequential
                      distribution patterns can be recognized for PSP pathology.
                      We evaluated heat maps and distribution patterns of
                      neuronal, astroglial, and oligodendroglial tau pathologies
                      and their combinations in different clinical subtypes of PSP
                      in postmortem brains. We used conditional probability and
                      logistic regression to model the sequential distribution of
                      tau pathologies across different brain regions. Tau
                      pathology uniformly predominates in the neurons of the
                      pallido-nigro-luysian axis in different clinical subtypes.
                      However, clinical subtypes are distinguished not only by
                      total tau load but rather cell-type (neuronal versus glial)
                      specific vulnerability patterns of brain regions suggesting
                      distinct dynamics or circuit-specific segregation of
                      propagation of tau pathologies. For Richardson syndrome
                      (n = 81) we recognize six sequential steps of
                      involvement of brain regions by the combination of cellular
                      tau pathologies. This is translated to six stages for the
                      practical neuropathological diagnosis by the evaluation of
                      the subthalamic nucleus, globus pallidus, striatum,
                      cerebellum with dentate nucleus, and frontal and occipital
                      cortices. This system can be applied to further clinical
                      subtypes by emphasizing whether they show caudal
                      (cerebellum/dentate nucleus) or rostral (cortical)
                      predominant, or both types of pattern. Defining
                      cell-specific stages of tau pathology helps to identify
                      preclinical or early-stage cases for the better
                      understanding of early pathogenic events, has implications
                      for understanding the clinical subtype-specific dynamics of
                      disease-propagation, and informs tau-neuroimaging on
                      distribution patterns.},
      keywords     = {Aged / Brain: pathology / Cohort Studies / Female / Humans
                      / Male / Middle Aged / Supranuclear Palsy, Progressive:
                      pathology / tau Proteins: analysis},
      cin          = {München common / AG Höglinger 1 / AG Levin},
      ddc          = {610},
      cid          = {I:(DE-2719)6000016 / I:(DE-2719)1110002 /
                      I:(DE-2719)1111016},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC7360645},
      pubmed       = {pmid:32383020},
      doi          = {10.1007/s00401-020-02158-2},
      url          = {https://pub.dzne.de/record/151075},
}