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@ARTICLE{Rubinski:268319,
      author       = {Rubinski, Anna and Dewenter, Anna and Zheng, Lukai and
                      Franzmeier, Nicolai and Stephenson, Henry and Deming,
                      Yuetiva and Duering, Marco and Gesierich, Benno and Denecke,
                      Jannis and Pham, An-Vi and Bendlin, Barbara and Ewers,
                      Michael},
      collaboration = {Initiative, Alzheimer’s Disease Neuroimaging},
      title        = {{F}lorbetapir {PET}-assessed demyelination is associated
                      with faster tau accumulation in an {APOE} ε4-dependent
                      manner.},
      journal      = {European journal of nuclear medicine and molecular imaging},
      volume       = {51},
      number       = {4},
      issn         = {1619-7070},
      address      = {Heidelberg [u.a.]},
      publisher    = {Springer-Verl.},
      reportid     = {DZNE-2024-00201},
      pages        = {1035 - 1049},
      year         = {2024},
      abstract     = {The main objectives were to test whether (1) a decrease in
                      myelin is associated with enhanced rate of fibrillar tau
                      accumulation and cognitive decline in Alzheimer's disease,
                      and (2) whether apolipoprotein E (APOE) ε4 genotype is
                      associated with worse myelin decrease and thus tau
                      accumulation.To address our objectives, we repurposed
                      florbetapir-PET as a marker of myelin in the white matter
                      (WM) based on previous validation studies showing that
                      beta-amyloid (Aβ) PET tracers bind to WM myelin. We
                      assessed 43 Aβ-biomarker negative (Aβ-) cognitively normal
                      participants and 108 Aβ+ participants within the AD
                      spectrum with florbetapir-PET at baseline and longitudinal
                      flortaucipir-PET as a measure of fibrillar tau (tau-PET)
                      over ~ 2 years. In linear regression analyses, we tested
                      florbetapir-PET in the whole WM and major fiber tracts as
                      predictors of tau-PET accumulation in a priori defined
                      regions of interest (ROIs) and fiber-tract projection areas.
                      In mediation analyses we tested whether tau-PET accumulation
                      mediates the effect of florbetapir-PET in the whole WM on
                      cognition. Finally, we assessed the role of myelin
                      alteration on the association between APOE and tau-PET
                      accumulation.Lower florbetapir-PET in the whole WM or at a
                      given fiber tract was predictive of faster tau-PET
                      accumulation in Braak stages or the connected grey matter
                      areas in Aβ+ participants. Faster tau-PET accumulation in
                      higher cortical brain areas mediated the association between
                      a decrease in florbetapir-PET in the WM and a faster rate of
                      decline in global cognition and episodic memory. APOE ε4
                      genotype was associated with a worse decrease in the whole
                      WM florbetapir-PET and thus enhanced tau-PET
                      accumulation.Myelin alterations are associated in an APOE
                      ε4 dependent manner with faster tau progression and
                      cognitive decline, and may therefore play a role in the
                      etiology of AD.},
      keywords     = {Humans / Apolipoprotein E4: genetics / Alzheimer Disease:
                      diagnostic imaging / Alzheimer Disease: genetics / Alzheimer
                      Disease: metabolism / Amyloid beta-Peptides: metabolism /
                      Apolipoproteins E / Brain: metabolism / Cognitive
                      Dysfunction: metabolism / Demyelinating Diseases: metabolism
                      / tau Proteins: metabolism / Positron-Emission Tomography /
                      Aniline Compounds / Ethylene Glycols / APOE (Other) /
                      Florbetapir-PET (Other) / Myelin (Other) / Tau (Other) /
                      Apolipoprotein E4 (NLM Chemicals) / florbetapir (NLM
                      Chemicals) / Amyloid beta-Peptides (NLM Chemicals) /
                      Apolipoproteins E (NLM Chemicals) / tau Proteins (NLM
                      Chemicals) / Aniline Compounds (NLM Chemicals) / Ethylene
                      Glycols (NLM Chemicals)},
      cin          = {Clinical Research (Munich)},
      ddc          = {610},
      cid          = {I:(DE-2719)1111015},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC10881623},
      pubmed       = {pmid:38049659},
      doi          = {10.1007/s00259-023-06530-8},
      url          = {https://pub.dzne.de/record/268319},
}