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@ARTICLE{Gr:154248,
      author       = {Görß, Doreen and Kilimann, Ingo and Dyrba, Martin and
                      Nitsch, Sascha and Krause, Bernd and Teipel, Stefan},
      title        = {{LATE}: {N}icht jede {D}emenz ist {A}lzheimer –
                      {D}iskussion einer neuen {K}rankheitsentität am
                      {F}allbeispiel : {Z}um aktuellen {S}tand der
                      „limbic-predominant age-related {TDP}-43 encephalopathy“
                      ({LATE}).},
      journal      = {Der Nervenarzt},
      volume       = {92},
      number       = {1},
      issn         = {1433-0407},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DZNE-2021-00109},
      pages        = {18 - 26},
      year         = {2021},
      abstract     = {Limbic-predominant age-related TDP-43 (Transactivation
                      response(TAR)-DNA-binding protein 43 kDa) encephalopathy
                      (LATE) has recently been characterized as a distinct
                      neuropathological entity within the spectrum of dementia.
                      Neuropathological alterations in the sense of LATE were
                      already previously described as a comorbidity to Alzheimer's
                      disease (AD) and it has been diagnosed independently from AD
                      pathology in autopsy studies since 2008. The framework of
                      LATE would account for the pathogenetic impact of limbic
                      TDP-43 proteinopathy as a driver of amnestic dementia,
                      either together with comorbid typical AD changes or as
                      a distinct feature. The LATE possibly explains divergent
                      clinical observations and biomarker results in patients
                      suffering from severe amnestic impairment without biomarker
                      evidence of AD-related amyloid and tau alterations. Whether
                      LATE represents a distinct neuropathological entity or is
                      part of the spectrum of neurodegenerative diseases
                      associated with TDP-43 is currently a matter of debate.
                      Further studies on the role of TDP-43 in the development of
                      amnestic dementia are urgently needed. Thus, the enrichment
                      of an amnestic phenotype in amyloid-centered therapeutic
                      drug studies bears the risk of higher rates of patients with
                      TDP-43 comorbidity, which could hinder the proof of efficacy
                      in such trials. This article presents the current state of
                      the discussion on LATE and illustrates the concept and the
                      clinical considerations with a case study.},
      keywords     = {Alzheimer Disease: diagnosis / Alzheimer Disease:
                      epidemiology / DNA-Binding Proteins: genetics / Humans /
                      TDP-43 Proteinopathies: genetics / Alzheimer’s disease
                      (Other) / Dementia (Other) / Proteinopathy (Other) / SNAP
                      (Other) / TDP-43 (Other) / DNA-Binding Proteins (NLM
                      Chemicals) / TARDBP protein, human (NLM Chemicals)},
      cin          = {AG Teipel},
      ddc          = {610},
      cid          = {I:(DE-2719)1510100},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32409844},
      pmc          = {pmc:PMC7809002},
      doi          = {10.1007/s00115-020-00922-z},
      url          = {https://pub.dzne.de/record/154248},
}