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@ARTICLE{McDade:281435,
      author       = {McDade, Eric M and Barthélemy, Nicolas R and Wang, Guoqiao
                      and Li, Yan and Cao, Yuchen and Gordon, Brian and Benzinger,
                      Tammie L S and Clifford, David and Goate, Alison M and
                      Renton, Alan E and Hassenstab, Jason and Llibre-Guerra,
                      Jorge J and Perrin, Richard J and Xiong, Chengjie and
                      Cruchaga, Carlos and Mummery, Catherine J and Berman, Sarah
                      B and Lah, James and Roberson, Erik D and Van Dyck,
                      Christopher and Gauthier, Serge and Masters, Colin L and
                      Masellis, Mario and Bittner, Tobias and Yaari, Roy and
                      Chhatwal, Jasmeer and Chrem, Patricio and Brooks, William
                      and Suzuki, Kazushi and Levin, Johannes J and Jucker,
                      Mathias and Ringman, John and Wallon, David and Ikeuchi,
                      Takeshi and Lee, Jae-Hong and Roh, Jee Hoon and Schofield,
                      Peter and Fox, Nick C and Ryan, Natalie S and Vöglein,
                      Jonathan and Karch, Celeste and Ibáñez, Laura and Day,
                      Gregory S and Sánchez-Valle, Raquel and Daniels, Alisha and
                      Morris, John C and Supnet-Bell, Charlene and Levey, Allan I
                      and Bateman, Randall J and Team, DIAN-TU Study},
      collaboration = {Team, DIAN Obs},
      title        = {{T}he relationship of soluble tau species with
                      {A}lzheimer's disease amyloid plaque removal and tau
                      pathology.},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {9},
      issn         = {1552-5260},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {DZNE-2025-01120},
      pages        = {e70689},
      year         = {2025},
      abstract     = {Tau-derived cerebrospinal fluid (CSF) biomarkers correlate
                      with amyloid-beta (Aβ) plaques or tau tangles in
                      Alzheimer's disease (AD). This study assessed the effects of
                      long-term anti-Aβ antibodies on amyloid plaques, tau
                      tangles, and CSF tau species to determine the relationships
                      between them.A post-hoc analysis of the DIAN-TU-001 trial
                      (NCT01760005) examined 142 participants at risk for
                      dominantly inherited AD randomized to solanezumab (n = 50),
                      gantenerumab (n = 52), or placebo (n = 40). High-resolution
                      mass spectrometry quantified CSF tau species over four
                      years.Phosphorylated tau (p-tau) species (153, 181, 217,
                      231) increased early in preclinical AD but were reduced with
                      gantenerumab-mediated Aβ plaque reduction. Nearly a decade
                      later, MTBR-tau243 and p-tau205 increased, showing no
                      association with Aβ reduction, aligning with tau tangle
                      pathology progression.Initially changing soluble p-tau
                      species track Aβ plaque reduction, while ptau205 and
                      MTBR-243 reflect tau tangle pathology, informing different
                      pathways of therapeutic strategies.p-tau217 and p-tau231
                      correlate with Aβ-PET and respond to Aβ-plaque lowering
                      therapies. Aβ immunotherapy trials support a direct link
                      between p-tau changes and Aβ plaques Gantenerumab reduces
                      Aβ plaques but does not affect tau NFT-related biomarkers.
                      Blood-based p-tau217 assays may provide a non-invasive tool
                      to monitor Aβ therapies. MTBR-tau243 strongly correlates
                      with tau PET and tracks NFT pathology progression. Further
                      studies are needed to validate tau biomarkers for tracking
                      NFT-targeting therapies.},
      keywords     = {Humans / tau Proteins: cerebrospinal fluid / Alzheimer
                      Disease: cerebrospinal fluid / Alzheimer Disease: pathology
                      / Alzheimer Disease: drug therapy / Plaque, Amyloid:
                      pathology / Plaque, Amyloid: drug therapy / Plaque, Amyloid:
                      cerebrospinal fluid / Male / Antibodies, Monoclonal,
                      Humanized: therapeutic use / Female / Biomarkers:
                      cerebrospinal fluid / Amyloid beta-Peptides /
                      Phosphorylation / Middle Aged / Aged / amyloid beta plaque
                      reduction (Other) / dominantly inherited Alzheimer's disease
                      (Other) / microtubule‐binding region (Other) /
                      phosphorylated tau (Other) / tau Proteins (NLM Chemicals) /
                      Antibodies, Monoclonal, Humanized (NLM Chemicals) /
                      Biomarkers (NLM Chemicals) / Amyloid beta-Peptides (NLM
                      Chemicals) / gantenerumab (NLM Chemicals) / solanezumab (NLM
                      Chemicals)},
      cin          = {Clinical Research (Munich) / AG Levin / AG Jucker},
      ddc          = {610},
      cid          = {I:(DE-2719)1111015 / I:(DE-2719)1111016 /
                      I:(DE-2719)1210001},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40985290},
      doi          = {10.1002/alz.70689},
      url          = {https://pub.dzne.de/record/281435},
}