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@ARTICLE{Scherr:140978,
      author       = {Scherr, Martin and Utz, Lukas and Tahmasian, Masoud and
                      Pasquini, Lorenzo and Grothe, Michel J and Rauschecker,
                      Josef P and Grimmer, Timo and Drzezga, Alexander and Sorg,
                      Christian and Riedl, Valentin},
      title        = {{E}ffective connectivity in the default mode network is
                      distinctively disrupted in {A}lzheimer's disease-{A}
                      simultaneous resting-state {FDG}-{PET}/f{MRI} study.},
      journal      = {Human brain mapping},
      volume       = {42},
      number       = {13},
      issn         = {1065-9471},
      address      = {New York, NY},
      publisher    = {Wiley-Liss},
      reportid     = {DZNE-2020-07300},
      pages        = {4134-4143},
      year         = {2021},
      abstract     = {A prominent finding of postmortem and molecular imaging
                      studies on Alzheimer's disease (AD) is the accumulation of
                      neuropathological proteins in brain regions of the default
                      mode network (DMN). Molecular models suggest that the
                      progression of disease proteins depends on the
                      directionality of signaling pathways. At network level,
                      effective connectivity (EC) reflects directionality of
                      signaling pathways. We hypothesized a specific pattern of EC
                      in the DMN of patients with AD, related to cognitive
                      impairment. Metabolic connectivity mapping is a novel
                      measure of EC identifying regions of signaling input based
                      on neuroenergetics. We simultaneously acquired resting-state
                      functional MRI and FDG-PET data from patients with early AD
                      (n = 35) and healthy subjects (n = 18) on an integrated
                      PET/MR scanner. We identified two distinct subnetworks of EC
                      in the DMN of healthy subjects: an anterior part with
                      bidirectional EC between hippocampus and medial prefrontal
                      cortex and a posterior part with predominant input into
                      medial parietal cortex. Patients had reduced input into the
                      medial parietal system and absent input from hippocampus
                      into medial prefrontal cortex (p < 0.05, corrected). In a
                      multiple linear regression with unimodal imaging and EC
                      measures (F4,25 = 5.63, p = 0.002, r2 = 0.47), we found that
                      EC (β = 0.45, p = 0.012) was stronger associated with
                      cognitive deficits in patients than any of the PET and fMRI
                      measures alone. Our approach indicates specific disruptions
                      of EC in the DMN of patients with AD and might be suitable
                      to test molecular theories about downstream and upstream
                      spreading of neuropathology in AD.},
      keywords     = {Aged / Alzheimer Disease: diagnostic imaging / Alzheimer
                      Disease: metabolism / Alzheimer Disease: physiopathology /
                      Cerebral Cortex: diagnostic imaging / Cerebral Cortex:
                      metabolism / Cerebral Cortex: physiopathology / Connectome:
                      methods / Default Mode Network: diagnostic imaging / Default
                      Mode Network: metabolism / Default Mode Network:
                      physiopathology / Humans / Magnetic Resonance Imaging:
                      methods / Multimodal Imaging: methods / Positron-Emission
                      Tomography: methods},
      cin          = {AG Teipel},
      ddc          = {610},
      cid          = {I:(DE-2719)1510100},
      pnm          = {344 - Clinical and Health Care Research (POF3-344) / 353 -
                      Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF3-344 / G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC8357005},
      pubmed       = {pmid:30697878},
      doi          = {10.1002/hbm.24517},
      url          = {https://pub.dzne.de/record/140978},
}