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@ARTICLE{Bischof:1037233,
      author       = {Bischof, Gérard N. and Jaeger, Elena and Giehl, Kathrin
                      and Jessen, Frank and Onur, Oezguer A. and O'Bryant, Sid and
                      Kara, Esra and Weiss, Peter H. and Drzezga, Alexander},
      title        = {{C}ortical {T}au {A}ggregation {P}atterns {A}ssociated
                      {W}ith {A}praxia in {P}atients {W}ith {A}lzheimer {D}isease},
      journal      = {Neurology},
      volume       = {103},
      number       = {12},
      issn         = {0028-3878},
      address      = {Philadelphia, Pa.},
      publisher    = {Wolters Kluwer},
      reportid     = {FZJ-2025-00566},
      pages        = {e210062},
      year         = {2024},
      note         = {A. Drzezga, G.N. Bischof, E. Jaeger, and P.H. Weiss are
                      fundedby the Deutsche Forschungsgemeinschaft -
                      Project-ID431549029 - SFB 1451. G.N. Bischof received
                      funding fromAlzheimer Forschung Initiative e.V., Germany
                      (AFI K1707).In addition, this study was supported by the
                      German ResearchFoundation (DFG, DR 445/9-1). Precursor for
                      the synthesisof the tracer [18F]PI-2620 was kindly provided
                      by Life Molecularimaging. The [18F]PI-2620 control sample
                      was kindlyprovided by SidO’Bryant and were taken from the
                      HABS-HDdatabase (apps.unthsc.edu/itr/studies/habs).
                      Researchreported on this publication was supported by the
                      NationalInstitute on Aging of the NIH under Award
                      NumbersR01AG054073, R01AG058533, P41EB015922,
                      andU19AG078109. The content is solely the responsibility of
                      theauthors and does not necessarily represent the official
                      views ofthe NIH.},
      abstract     = {Background and objectives: Apraxia is a frequently observed
                      symptom in Alzheimer disease (AD), but the causal
                      pathomechanism underlying this dysfunction is not well
                      understood. Previous studies have demonstrated associations
                      between various cognitive dysfunctions in AD and cortical
                      tau deposition in specific brain areas, suggesting a causal
                      relationship. Thus, we hypothesized that specific regional
                      patterns of tau pathology in praxis-related brain regions
                      may be associated with apraxic deficits in AD. For this
                      purpose, we performed PET imaging with the second-generation
                      tau-PET tracer [18F]PI-2620 in a well-defined group of
                      patients with AD (N = 33) who had been systematically
                      assessed for apraxia.Methods: Patients with a
                      biomarker-confirmed diagnosis of AD were recruited in
                      addition to a sample of cognitively unimpaired (CU1) control
                      participants. Both groups underwent apraxia assessments with
                      the Dementia Apraxia Screening Test. In addition, PET
                      imaging with [18F]PI-2620 was performed to assess tau
                      pathology in the patients with AD. To specifically
                      investigate the association of apraxia severity with
                      regional tau pathology, we compared the PET data from this
                      group with an independent sample of amyloid-negative
                      cognitively intact participants (CU2) by generation of
                      z-score deviation maps and submitted these maps to a
                      voxel-based multiple regression analysis.Results: A total of
                      120 participants $(39\%$ female) with a mean age of 67.9
                      (9.2) years were included in the study (AD = 33; CU1; N =
                      33; CU2; N = 54). We identified a significant correlation
                      between circumscribed clusters of tau aggregation in
                      praxis-related brain regions (including parietal (angular
                      gyrus), temporal, and occipital regions) and severity of
                      apraxia in patients with AD. By contrast, no significant
                      correlations between tau tracer uptake in primary motor
                      cortex or subcortical brain regions and apraxia were
                      observed.Discussion: These results suggest that tau
                      deposition in specific cortical praxis-related brain regions
                      may induce local neuronal dysfunction leading to a
                      dose-dependent functional decline in praxis performance in
                      AD. The awareness of this relationship could further refine
                      a differentiated individual diagnostic characterization and
                      classification of patients with AD.},
      cin          = {INM-3 / INM-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406 / I:(DE-Juel1)INM-2-20090406},
      pnm          = {5251 - Multilevel Brain Organization and Variability
                      (POF4-525) / DFG project G:(GEPRIS)431549029 - SFB 1451:
                      Schlüsselmechanismen normaler und krankheitsbedingt
                      gestörter motorischer Kontrolle (431549029) / 5252 - Brain
                      Dysfunction and Plasticity (POF4-525) / 5253 - Neuroimaging
                      (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5251 / G:(GEPRIS)431549029 /
                      G:(DE-HGF)POF4-5252 / G:(DE-HGF)POF4-5253},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {39626130},
      UT           = {WOS:001370437800001},
      doi          = {10.1212/WNL.0000000000210062},
      url          = {https://juser.fz-juelich.de/record/1037233},
}