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@ARTICLE{Oeckl:277978,
      author       = {Oeckl, Patrick and Mayer, Benjamin and Bateman, Randall J
                      and Day, Gregory S and Fox, Nick C and Huey, Edward D and
                      Ibanez, Laura and Ikeuchi, Takeshi and Jucker, Mathias and
                      Lee, Jae-Hong and Levin, Johannes and Llibre-Guerra, Jorge J
                      and Lopera, Francisco and McDade, Eric and Morris, John C
                      and Niimi, Yoshiki and Roh, Jee Hoon and Sánchez-Valle,
                      Raquel and Schofield, Peter R and Otto, Markus},
      collaboration = {Network, Dominantly Inherited Alzheimer},
      title        = {{E}arly increase of the synaptic blood marker β-synuclein
                      in asymptomatic autosomal dominant {A}lzheimer's disease.},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {4},
      issn         = {1552-5260},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {DZNE-2025-00510},
      pages        = {e70146},
      year         = {2025},
      abstract     = {β-synuclein is a promising blood marker to track synaptic
                      degeneration in Alzheimer's disease (AD) but changes in
                      preclinical AD are unclear.We investigated serum
                      β-synuclein in 69 cognitively unimpaired mutation
                      non-carriers, 78 cognitively unimpaired AD mutation carriers
                      (asymptomatic AD), and 31 symptomatic mutation carriers from
                      the Dominantly Inherited Alzheimer Network.β-synuclein
                      levels were already higher in asymptomatic AD mutation
                      carriers compared to non-carriers and highest in symptomatic
                      carriers. Longitudinal trajectories and correlation analyses
                      indicated that β-synuclein levels start to rise after
                      amyloid deposition preceding axonal degeneration, brain
                      atrophy and hypometabolism, and cognitive decline.
                      β-synuclein levels were associated with cognitive
                      impairment and gradually increased with declining
                      cognition.Our study supports the use of blood β-synuclein
                      to track synaptic changes in preclinical AD and as a
                      surrogate marker for cognitive impairment which might be
                      used in early diagnosis and to support patient selection and
                      monitoring of treatment effects in clinical trials.Blood
                      β-synuclein levels were already higher in asymptomatic
                      Alzheimer's disease (AD) mutation carriers. Blood
                      β-synuclein levels were highest in symptomatic AD mutation
                      carriers. Blood β-synuclein levels start to rise 11 years
                      before symptom onset. Rise of β-synuclein precedes axonal
                      degeneration, brain atrophy, and cognitive decline.
                      β-synuclein levels gradually increased with declining
                      cognition.},
      keywords     = {Humans / Alzheimer Disease: genetics / Alzheimer Disease:
                      blood / Alzheimer Disease: pathology / Male / Female /
                      Biomarkers: blood / Middle Aged / Mutation: genetics /
                      beta-Synuclein: blood / Aged / Brain: pathology / Brain:
                      diagnostic imaging / Synapses / Cognitive Dysfunction: blood
                      / Longitudinal Studies / asymptomatic mutation carriers
                      (Other) / autosomal dominant Alzheimer´s disease (Other) /
                      blood biomarker (Other) / preclinical Alzheimer´s disease
                      (Other) / synaptic degeneration (Other) / β‐synuclein
                      (Other) / Biomarkers (NLM Chemicals) / beta-Synuclein (NLM
                      Chemicals)},
      cin          = {AG Öckl / AG Jucker / AG Levin / Clinical Research
                      (Munich)},
      ddc          = {610},
      cid          = {I:(DE-2719)5000073 / I:(DE-2719)1210001 /
                      I:(DE-2719)1111016 / I:(DE-2719)1111015},
      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},
      experiment   = {EXP:(DE-2719)DIAN-20090101},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40207431},
      doi          = {10.1002/alz.70146},
      url          = {https://pub.dzne.de/record/277978},
}