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@ARTICLE{Stocker:168699,
      author       = {H. Stocker$^*$ and A. Nabers and L. Perna and T.
                      Möllers$^*$ and D. Rujescu and A. M. Hartmann and B.
                      Holleczek and B. Schöttker$^*$ and J. Stockmann and K.
                      Gerwert and H. Brenner$^*$},
      title        = {{G}enetic predisposition, {A}β misfolding in blood plasma,
                      and {A}lzheimer's disease.},
      journal      = {Translational Psychiatry},
      volume       = {11},
      number       = {1},
      issn         = {2158-3188},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2021-01007},
      pages        = {261},
      year         = {2021},
      note         = {#EA:C070#LA:C070#},
      abstract     = {Alzheimer's disease is highly heritable and characterized
                      by amyloid plaques and tau tangles in the brain. The aim of
                      this study was to investigate the association between
                      genetic predisposition, Aβ misfolding in blood plasma, a
                      unique marker of Alzheimer associated neuropathological
                      changes, and Alzheimer's disease occurrence within 14 years.
                      Within a German community-based cohort, two polygenic risk
                      scores (clinical Alzheimer's disease and Aβ42 based) were
                      calculated, APOE genotype was determined, and Aβ misfolding
                      in blood plasma was measured by immuno-infrared sensor in 59
                      participants diagnosed with Alzheimer's disease during 14
                      years of follow-up and 581 participants without dementia
                      diagnosis. Associations between each genetic marker and Aβ
                      misfolding were assessed through logistic regression and the
                      ability of each genetic marker and Aβ misfolding to predict
                      Alzheimer's disease was determined. The Alzheimer's disease
                      polygenic risk score and APOE ε4 presence were associated
                      to Aβ misfolding (odds ratio, $95\%$ confidence interval:
                      per standard deviation increase of score: 1.25, 1.03-1.51;
                      APOE ε4 presence: 1.61, 1.04-2.49). No association was
                      evident for the Aβ polygenic risk score. All genetic
                      markers were predictive of Alzheimer's disease diagnosis
                      albeit much less so than Aβ misfolding (areas under the
                      curve: Aβ polygenic risk score: 0.55; AD polygenic risk
                      score: 0.59; APOE ε4: 0.63; Aβ misfolding: 0.84). Clinical
                      Alzheimer's genetic risk was associated to early
                      pathological changes (Aβ misfolding) measured in blood,
                      however, predicted Alzheimer's disease less accurately than
                      Aβ misfolding itself. Genetic predisposition may provide
                      information regarding disease initiation, while Aβ
                      misfolding could be important in clinical risk prediction.},
      cin          = {C070},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33934115},
      doi          = {10.1038/s41398-021-01380-0},
      url          = {https://inrepo02.dkfz.de/record/168699},
}