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@ARTICLE{Schultz:283157,
      author       = {Schultz, Stephanie A and Rao, Yiwen and Liu, Lei and
                      Ostaszewski, Beth and Anderson, Amirah K and Yau, Wai-Ying
                      Wendy and Shirzadi, Zahra and Gordon, Brian A and
                      Hassenstab, Jason and Morris, John C and Perrin, Richard J
                      and Allegri, Ricardo F and Barthélemy, Nicolas R and Fox,
                      Nick and Day, Gregory S and Jucker, Mathias and Levey, Allan
                      I and Levin, Johannes and Mori, Hiroshi and Salloway,
                      Stephen and Schofield, Peter and McDade, Eric and Sperling,
                      Reisa A and Bateman, Randall J and Selkoe, Dennis J and
                      Chhatwal, Jasmeer P},
      collaboration = {Network, and the Dominantly Inherited Alzheimer's},
      title        = {{P}lasma levels of an {N}-terminal tau fragment predict
                      {A}lzheimer's and neurodegenerative disease biomarkers in
                      autosomal dominant {A}lzheimer's disease.},
      journal      = {Alzheimer's and dementia},
      volume       = {22},
      number       = {1},
      issn         = {1552-5260},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {DZNE-2026-00053},
      pages        = {e71049},
      year         = {2026},
      abstract     = {Tau species lacking truncation of the N-terminal region,
                      including plasma N-terminal tau fragment 1 (NT1), have been
                      previously associated with cognitive decline,
                      neurodegeneration, and tau pathology in late-onset sporadic
                      Alzheimer's disease (AD).Here, we examined cross-sectional
                      and longitudinal plasma NT1 as a possible predictor of
                      cognitive, clinical, and core AD biomarker trajectories in
                      autosomal dominant AD (ADAD).NT1 levels in ADAD mutation
                      carriers (MC; n = 132) increased across the disease
                      continuum, compared to non-carriers (NC; n = 75), becoming
                      elevated about a decade prior to estimated symptom onset.
                      Cross-sectional and longitudinal NT1 levels in MC were
                      associated with clinical, cognitive, and biomarker changes.
                      NT1 increases continued in symptomatic phases of disease, a
                      distinct trajectory from that seen with CSF p-tau217 and
                      other phospho-tau species.Together, our results suggest that
                      plasma NT1-alone or combined with other tau measures-may be
                      useful in studying AD-related clinical, cognitive, and
                      biomarker outcomes.Leveraging a deeply phenotyped cohort of
                      individuals carrying a pathogenic variant for autosomal
                      dominant Alzheimer's disease (ADAD) and their non-carrier
                      family members, our results suggest that plasma N-terminal
                      tau fragment 1 (NT1) levels mirrored changes in clinical,
                      cognitive, and neurodegenerative measures in ADAD,
                      particularly in late asymptomatic and early symptomatic
                      phases of disease. NT1 levels correlated with cerebrospinal
                      fluid (CSF) measures of tau pathology but less so with CSF
                      or imaging measures of β-amyloid pathology. Together with
                      previous supportive findings in preclinical and symptomatic
                      sporadic AD, these results suggest that plasma NT1-alone or
                      combined with other tau measures-may be useful in studying
                      AD-related tau pathology and neurodegeneration across a wide
                      spectrum of disease.},
      keywords     = {Humans / tau Proteins: blood / Alzheimer Disease: blood /
                      Alzheimer Disease: genetics / Alzheimer Disease: diagnosis /
                      Biomarkers: blood / Male / Female / Cross-Sectional Studies
                      / Middle Aged / Longitudinal Studies / Peptide Fragments:
                      blood / Aged / Neurodegenerative Diseases: blood / ADAD
                      (Other) / biomarker (Other) / neurodegeneration (Other) /
                      tauopathy (Other) / tau Proteins (NLM Chemicals) /
                      Biomarkers (NLM Chemicals) / Peptide Fragments (NLM
                      Chemicals) / MAPT protein, human (NLM Chemicals)},
      cin          = {AG Jucker / Clinical Research (Munich) / AG Levin},
      ddc          = {610},
      cid          = {I:(DE-2719)1210001 / I:(DE-2719)1111015 /
                      I:(DE-2719)1111016},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
                      Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
      experiment   = {EXP:(DE-2719)DIAN-20090101},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41505233},
      doi          = {10.1002/alz.71049},
      url          = {https://pub.dzne.de/record/283157},
}