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@ARTICLE{Stockbauer:268317,
author = {Stockbauer, Anna and Beyer, Leonie and Huber, Maria and
Kreuzer, Annika and Palleis, Carla and Katzdobler, Sabrina
and Rauchmann, Boris Stephan and Morbelli, Silvia and
Chincarini, Andrea and Bruffaerts, Rose and Vandenberghe,
Rik and Kramberger, Milica G and Trost, Maja and Garibotto,
Valentina and Nicastro, Nicolas and Lathuilière, Aurélien
and Lemstra, Afina W and van Berckel, Bart N M and Pilotto,
Andrea and Padovani, Alessandro and Ochoa-Figueroa, Miguel A
and Davidsson, Anette and Camacho, Valle and Peira, Enrico
and Bauckneht, Matteo and Pardini, Matteo and Sambuceti,
Gianmario and Aarsland, Dag and Nobili, Flavio and Gross,
Mattes and Vöglein, Jonathan and Perneczky, Robert and
Pogarell, Oliver and Buerger, Katharina and Franzmeier,
Nikolai and Danek, Adrian and Levin, Johannes and
Höglinger, Günter U and Bartenstein, Peter and Cumming,
Paul and Rominger, Axel and Brendel, Matthias},
title = {{M}etabolic network alterations as a supportive biomarker
in dementia with {L}ewy bodies with preserved dopamine
transmission.},
journal = {European journal of nuclear medicine and molecular imaging},
volume = {51},
number = {4},
issn = {1619-7070},
address = {Heidelberg [u.a.]},
publisher = {Springer-Verl.},
reportid = {DZNE-2024-00199},
pages = {1023 - 1034},
year = {2024},
abstract = {Metabolic network analysis of FDG-PET utilizes an index of
inter-regional correlation of resting state glucose
metabolism and has been proven to provide complementary
information regarding the disease process in parkinsonian
syndromes. The goals of this study were (i) to evaluate
pattern similarities of glucose metabolism and network
connectivity in dementia with Lewy bodies (DLB) subjects
with subthreshold dopaminergic loss compared to advanced
disease stages and to (ii) investigate metabolic network
alterations of FDG-PET for discrimination of patients with
early DLB from other neurodegenerative disorders
(Alzheimer's disease, Parkinson's disease, multiple system
atrophy) at individual patient level via principal component
analysis (PCA).FDG-PETs of subjects with probable or
possible DLB (n = 22) without significant dopamine
deficiency (z-score < 2 in putamen binding loss on DaT-SPECT
compared to healthy controls (HC)) were scaled by
global-mean, prior to volume-of-interest-based analyses of
relative glucose metabolism. Single region metabolic changes
and network connectivity changes were compared against HC (n
= 23) and against DLB subjects with significant dopamine
deficiency (n = 86). PCA was applied to test discrimination
of patients with DLB from disease controls (n = 101) at
individual patient level.Similar patterns of hypo-
(parietal- and occipital cortex) and hypermetabolism (basal
ganglia, limbic system, motor cortices) were observed in DLB
patients with and without significant dopamine deficiency
when compared to HC. Metabolic connectivity alterations
correlated between DLB patients with and without significant
dopamine deficiency (R2 = 0.597, p < 0.01). A PCA trained by
DLB patients with dopamine deficiency and HC discriminated
DLB patients without significant dopaminergic loss from
other neurodegenerative parkinsonian disorders at individual
patient level (area-under-the-curve (AUC):
0.912).Disease-specific patterns of altered glucose
metabolism and altered metabolic networks are present in DLB
subjects without significant dopaminergic loss. Metabolic
network alterations in FDG-PET can act as a supporting
biomarker in the subgroup of DLB patients without
significant dopaminergic loss at symptoms onset.},
keywords = {Humans / Lewy Body Disease: diagnostic imaging / Dopamine:
metabolism / Fluorodeoxyglucose F18 / Alzheimer Disease:
metabolism / Positron-Emission Tomography / Glucose:
metabolism / Metabolic Networks and Pathways / DaT-Scan
(Other) / Dementia with Lewy bodies (Other) / FDG-PET
(Other) / Metabolic connectivity (Other) / Dopamine (NLM
Chemicals) / Fluorodeoxyglucose F18 (NLM Chemicals) /
Glucose (NLM Chemicals)},
cin = {AG Haass / AG Simons / Clinical Research (Munich) / AG
Dichgans},
ddc = {610},
cid = {I:(DE-2719)1110007 / I:(DE-2719)1110008 /
I:(DE-2719)1111015 / I:(DE-2719)5000022},
pnm = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pmc = {pmc:PMC10881642},
pubmed = {pmid:37971501},
doi = {10.1007/s00259-023-06493-w},
url = {https://pub.dzne.de/record/268317},
}