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@ARTICLE{Steidel:909234,
      author       = {Steidel, Kenan and Ruppert, Marina C. and Greuel, Andrea
                      and Tahmasian, Masoud and Maier, Franziska and Hammes,
                      Jochen and van Eimeren, Thilo and Timmermann, Lars and
                      Tittgemeyer, Marc and Drzezga, Alexander and Pedrosa, David
                      J. and Eggers, Carsten},
      title        = {{L}ongitudinal trimodal imaging of midbrain-associated
                      network degeneration in {P}arkinson’s disease},
      journal      = {npj Parkinson's Disease},
      volume       = {8},
      number       = {1},
      issn         = {2373-8057},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {FZJ-2022-03078},
      pages        = {79},
      year         = {2022},
      abstract     = {The prevailing network perspective of Parkinson's disease
                      (PD) emerges not least from the ascending neuropathology
                      traceable in histological studies. However, whether
                      longitudinal in vivo correlates of network degeneration in
                      PD can be observed remains unresolved. Here, we applied a
                      trimodal imaging protocol combining 18F-fluorodeoxyglucose
                      (FDG)- and 18F-fluoro-L-Dopa- (FDOPA)-PET with resting-state
                      functional MRI to assess longitudinal changes in midbrain
                      metabolism, striatal dopamine depletion and striatocortical
                      dysconnectivity in 17 well-characterized PD patients.
                      Whole-brain (un)paired-t-tests with focus on midbrain or
                      striatum were performed between visits and in relation to 14
                      healthy controls (HC) in PET modalities. Resulting clusters
                      of FDOPA-PET comparisons provided volumes for seed-based
                      functional connectivity (FC) analyses between visits and in
                      relation to HC. FDG metabolism in the left midbrain
                      decreased compared to baseline along with caudatal
                      FDOPA-uptake. This caudate cluster exhibited a longitudinal
                      FC decrease to sensorimotor and frontal areas. Compared to
                      healthy subjects, dopamine-depleted putamina indicated
                      stronger decline in striatocortical FC at follow-up with
                      respect to baseline. Increasing nigrostriatal deficits and
                      striatocortical decoupling were associated with
                      deterioration in motor scores between visits in
                      repeated-measures correlations. In summary, our results
                      demonstrate the feasibility of in-vivo tracking of
                      progressive network degeneration using a multimodal imaging
                      approach. Specifically, our data suggest advancing striatal
                      and widespread striatocortical dysfunction via an
                      anterior-posterior gradient originating from a hypometabolic
                      midbrain cluster within a well-characterized and only mild
                      to moderately affected PD cohort during a relatively short
                      period.},
      cin          = {INM-7 / INM-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-7-20090406 / I:(DE-Juel1)INM-2-20090406},
      pnm          = {5253 - Neuroimaging (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5253},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {35732679},
      UT           = {WOS:000814627900001},
      doi          = {10.1038/s41531-022-00341-8},
      url          = {https://juser.fz-juelich.de/record/909234},
}