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@INPROCEEDINGS{Biel:283095,
      author       = {Biel, Davina and Steward, Anna and Dewenter, Anna and
                      Dehsarvi, Amir and Zhu, Zeyu and Roemer-Cassiano, Sebastian
                      and Frontzkowski, Lukas and Hirsch, Fabian and Brendel,
                      Matthias and Franzmeier, Nicolai},
      title        = {{P}lasma p‐tau217 as a suitable biomarker for monitoring
                      cognitive changes in {A}lzheimer’s disease},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {Suppl 8},
      issn         = {1552-5260},
      reportid     = {DZNE-2025-01502},
      pages        = {e110180},
      year         = {2025},
      abstract     = {With the approval of anti-amyloid therapies in Alzheimer's
                      disease (AD), surrogate biomarkers are urgently needed to
                      monitor treatment effects that translate into clinical
                      benefits. Candidate biomarkers, including amyloid-PET,
                      tau-PET, plasma phosphorylated tau (p-tau), and MRI-assessed
                      atrophy, capture core pathophysiological changes in AD.
                      While cross-sectional biomarker assessments are critical for
                      diagnosis and staging, biomarker change rates may better
                      reflect disease dynamics, making them more suitable for
                      monitoring treatment efficacy. Therefore, we determined
                      which biomarker most effectively tracks cognitive changes in
                      AD, identifying those best suited for efficient monitoring
                      of disease-modifying treatments.We leveraged ADNI (N = 108)
                      and A4 (N = 151) participants with longitudinal AD biomarker
                      data (global amyloid-PET, temporal meta tau-PET, plasma
                      p-tau217, MRI-assessed cortical thickness in the AD
                      signature region) together with cognitive assessments (ADNI:
                      MMSE, ADAS13, CDR-SB; A4: MMSE, PACC). Linear mixed models
                      were used to calculate change rates for biomarkers and
                      cognition. To test whether biomarker changes track cognitive
                      decline, linear models were applied, to test biomarker
                      change rates as a predictor of cognitive change rates.
                      Standardized beta values from bootstrapped linear models
                      were extracted to compare the strengths of correlations
                      between biomarkers and cognitive decline. For non-parametric
                      comparisons, $95\%$ confidence intervals (CIs) of
                      standardized beta values were compared. Models were
                      controlled for age, sex, education, and baseline cognition,
                      with ADNI models additionally adjusted for clinical
                      status.In both cohorts, changes in temporal tau-PET, plasma
                      p-tau217, and MRI-assessed cortical thickness were
                      associated with cognitive decline (ADNI: Figure 1; A4:
                      Figure 2). Amyloid-PET changes showed no significant
                      association with cognitive changes (ADNI: Figure 1A+F+K; A4:
                      Figure 2A+F). Bootstrapping confirmed that tau-PET, plasma
                      p-tau217, and cortical thickness track cognitive decline,
                      but not amyloid-PET (ADNI: Figure 1E+J+O; A4: Figure 2E+J).
                      Overlapping CIs for tau-PET and plasma p-tau217 indicated
                      comparable predictive accuracy.Our findings demonstrate that
                      tau-PET and plasma p-tau217 are robust biomarkers for
                      monitoring cognitive changes, with plasma p-tau217 offering
                      a cost-effective, scalable alternative for clinical use.
                      Changes in amyloid-PET do not reliably reflect cognitive
                      decline, limiting its utility as a treatment monitoring
                      tool. Although cortical thickness correlates with cognitive
                      changes, its application is limited by pseudoatrophy and
                      volume loss induced by anti-amyloid antibody treatments.},
      month         = {Jul},
      date          = {2025-07-27},
      organization  = {Alzheimer’s Association
                       International Conference, Toronto
                       (Canada), 27 Jul 2025 - 31 Jul 2025},
      keywords     = {Humans / Alzheimer Disease: diagnostic imaging / Alzheimer
                      Disease: pathology / Male / Female / tau Proteins: blood /
                      Biomarkers: blood / Aged / Magnetic Resonance Imaging /
                      Positron-Emission Tomography / Longitudinal Studies / Aged,
                      80 and over / Brain: diagnostic imaging / Brain: pathology /
                      Amyloid beta-Peptides / tau Proteins (NLM Chemicals) /
                      Biomarkers (NLM Chemicals) / Amyloid beta-Peptides (NLM
                      Chemicals)},
      cin          = {AG Haass},
      ddc          = {610},
      cid          = {I:(DE-2719)1110007},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)1 / PUB:(DE-HGF)16},
      pubmed       = {pmid:41433469},
      pmc          = {pmc:PMC12725594},
      doi          = {10.1002/alz70862_110180},
      url          = {https://pub.dzne.de/record/283095},
}