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@ARTICLE{Louwersheimer:138696,
      author       = {Louwersheimer, Eva and Wolfsgruber, Steffen and Espinosa,
                      Ana and Lacour, André and Heilmann-Heimbach, Stefanie and
                      Alegret, Montserrat and Hernández, Isabel and Rosende-Roca,
                      Maitée and Tárraga, Lluís and Boada, Mercè and
                      Kornhuber, Johannes and Peters, Oliver and Frölich, Lutz
                      and Hüll, Michael and Rüther, Eckart and Wiltfang, Jens
                      and Scherer, Martin and Riedel-Heller, Steffi and Jessen,
                      Frank and Nöthen, Markus M and Maier, Wolfgang and Koene,
                      Ted and Scheltens, Philip and Holstege, Henne and Wagner,
                      Michael and Ruiz, Agustín and van der Flier, Wiesje M and
                      Becker, Tim and Ramirez, Alfredo},
      title        = {{A}lzheimer's disease risk variants modulate endophenotypes
                      in mild cognitive impairment.},
      journal      = {Alzheimer's and dementia},
      volume       = {12},
      number       = {8},
      issn         = {1552-5260},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-05018},
      pages        = {872-881},
      year         = {2016},
      abstract     = {We evaluated the effect of Alzheimer's disease (AD)
                      susceptibility loci on endophenotypes closely related with
                      AD pathology in patients with mild cognitive impairment
                      (MCI).We selected 1730 MCI patients from four independent
                      data sets. Weighted polygenic risk scores (PGS) were
                      constructed of 18 non-apolipoprotein E (APOE) AD risk
                      variants. In addition, we determined APOE genotype. AD
                      endophenotypes were cognitive decline over time and
                      cerebrospinal fluid (CSF) biomarkers (aβ, tau, ptau).PGS
                      was modestly associated with cognitive decline over time, as
                      measured by mini-mental state examination (MMSE) (β ±
                      SE:-0.24 ± 0.10; P = .012), and with CSF levels of tau
                      and ptau (tau: 1.38 ± 0.36, P = 1.21 × 10(-4); ptau:
                      1.40 ± 0.36, P = 1.02 × 10(-4)).In MCI, we observed a
                      joint effect of AD susceptibility loci on nonamyloid
                      endophenotypes, suggesting a link of these genetic loci with
                      neuronal degeneration in general rather than with
                      Alzheimer-related amyloid deposition.},
      keywords     = {Aged / Aged, 80 and over / Alzheimer Disease: cerebrospinal
                      fluid / Alzheimer Disease: diagnosis / Amyloid
                      beta-Peptides: cerebrospinal fluid / Apolipoproteins E:
                      genetics / Cognitive Dysfunction: cerebrospinal fluid /
                      Cognitive Dysfunction: complications / Cognitive
                      Dysfunction: genetics / Cohort Studies / Datasets as Topic:
                      statistics $\&$ numerical data / Endophenotypes:
                      cerebrospinal fluid / Female / Humans / Male / Mental Status
                      Schedule / Middle Aged / Multifactorial Inheritance:
                      genetics / Neuropsychological Tests / Odds Ratio /
                      Polymorphism, Single Nucleotide: genetics / Statistics,
                      Nonparametric / Amyloid beta-Peptides (NLM Chemicals) /
                      Apolipoproteins E (NLM Chemicals)},
      cin          = {AG Wagner / AG Becker ; GenomMathematik ; GenomMathematik /
                      U Clinical Researchers - Bonn},
      ddc          = {610},
      cid          = {I:(DE-2719)1011201 / I:(DE-2719)1013007 /
                      I:(DE-2719)7000001},
      pnm          = {344 - Clinical and Health Care Research (POF3-344) / 345 -
                      Population Studies and Genetics (POF3-345)},
      pid          = {G:(DE-HGF)POF3-344 / G:(DE-HGF)POF3-345},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26921674},
      doi          = {10.1016/j.jalz.2016.01.006},
      url          = {https://pub.dzne.de/record/138696},
}