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@ARTICLE{Caspers:864800,
      author       = {Caspers, Svenja and Röckner, Melanie E and Jockwitz,
                      Christiane and Bittner, Nora and Teumer, Alexander and
                      Herms, Stefan and Hoffmann, Per and Nöthen, Markus M and
                      Moebus, Susanne and Amunts, Katrin and Cichon, Sven and
                      Mühleisen, Thomas W},
      title        = {{P}athway-{S}pecific {G}enetic {R}isk for {A}lzheimer's
                      {D}isease {D}ifferentiates {R}egional {P}atterns of
                      {C}ortical {A}trophy in {O}lder {A}dults},
      journal      = {Cerebral cortex},
      volume       = {30},
      number       = {2},
      issn         = {1460-2199},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {FZJ-2019-04457},
      pages        = {801-811},
      year         = {2020},
      abstract     = {Brain aging is highly variable and represents a challenge
                      to delimit aging from disease processes. Moreover, genetic
                      factors may influence both aging and disease. Here we
                      focused on this issue and investigated effects of multiple
                      genetic loci previously identified to be associated with
                      late-onset Alzheimer's disease (AD) on brain structure of
                      older adults from a population sample. We calculated a
                      genetic risk score (GRS) using genome-wide significant
                      single-nucleotide polymorphisms from genome-wide association
                      studies of AD and tested its effect on cortical thickness
                      (CT). We observed a common pattern of cortical thinning
                      (right inferior frontal, left posterior temporal, medial
                      occipital cortex). To identify CT changes by specific
                      biological processes, we subdivided the GRS effect according
                      to AD-associated pathways and performed follow-up analyses.
                      The common pattern from the main analysis was further
                      differentiated by pathway-specific effects yielding a more
                      bilateral pattern. Further findings were located in the
                      superior parietal and mid/anterior cingulate regions
                      representing 2 unique pathway-specific patterns. All
                      patterns, except the superior parietal pattern, were
                      influenced by apolipoprotein E. Our step-wise approach
                      revealed atrophy patterns that partially resembled imaging
                      findings in early stages of AD. Our study provides evidence
                      that genetic burden for AD contributes to structural brain
                      variability in normal aging.},
      cin          = {INM-1},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-1-20090406},
      pnm          = {571 - Connectivity and Activity (POF3-571) / HBP SGA2 -
                      Human Brain Project Specific Grant Agreement 2 (785907)},
      pid          = {G:(DE-HGF)POF3-571 / G:(EU-Grant)785907},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31402375},
      UT           = {WOS:000530440700029},
      doi          = {10.1093/cercor/bhz127},
      url          = {https://juser.fz-juelich.de/record/864800},
}