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@ARTICLE{Holtbernd:200990,
author = {Holtbernd, F. and Ma, Y. and Peng, S. and Schwartz, F. and
Timmermann, L. and Kracht, L. and Fink, Gereon Rudolf and
Tang, C. C. and Eidelberg, D. and Eggers, C.},
title = {{D}opaminergic correlates of metabolic network activity in
{P}arkinson’s disease},
journal = {Human brain mapping},
volume = {36},
number = {9},
issn = {1065-9471},
address = {New York, NY},
publisher = {Wiley-Liss},
reportid = {FZJ-2015-03309},
pages = {3575 - 3585},
year = {2015},
abstract = {Parkinson's disease (PD) is associated with distinct
metabolic covariance patterns that relate to the motor and
cognitive manifestations of the disorder. It is not known,
however, how the expression of these patterns relates to
measurements of nigrostriatal dopaminergic activity from the
same individuals. To explore these associations, we studied
106 PD subjects who underwent cerebral PET with both
18F-fluorodeoxyglucose (FDG) and 18F-fluoro-L-dopa (FDOPA).
Expression values for the PD motor- and cognition-related
metabolic patterns (PDRP and PDCP, respectively) were
computed for each subject; these measures were correlated
with FDOPA uptake on a voxel-by-voxel basis. To explore the
relationship between dopaminergic function and local
metabolic activity, caudate and putamen FDOPA PET signal was
correlated voxel-wise with FDG uptake over the entire brain.
PDRP expression correlated with FDOPA uptake in caudate and
putamen (P < 0.001), while PDCP expression correlated
with uptake in the anterior striatum (P < 0.001). While
statistically significant, the correlations were only of
modest size, accounting for less than $20\%$ of the overall
variation in these measures. After controlling for PDCP
expression, PDRP correlations were significant only in the
posterior putamen. Of note, voxel-wise correlations between
caudate/putamen FDOPA uptake and whole-brain FDG uptake were
significant almost exclusively in PDRP regions. Overall, the
data indicate that PDRP and PDCP expression correlates
significantly with PET indices of presynaptic dopaminergic
functioning obtained in the same individuals. Even so, the
modest size of these correlations suggests that in PD
patients, individual differences in network activity cannot
be explained solely by nigrostriatal dopamine loss},
cin = {INM-3},
ddc = {610},
cid = {I:(DE-Juel1)INM-3-20090406},
pnm = {572 - (Dys-)function and Plasticity (POF3-572)},
pid = {G:(DE-HGF)POF3-572},
typ = {PUB:(DE-HGF)16},
UT = {WOS:000360209000019},
pubmed = {pmid:26037537},
doi = {10.1002/hbm.22863},
url = {https://juser.fz-juelich.de/record/200990},
}