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DOI: 10.1055/s-0039-1683498
Striatal dopamine deficiency is associated with increased striatal glucose metabolism in Dementia with Lewy Bodies
Publikationsverlauf
Publikationsdatum:
27. März 2019 (online)
Ziel/Aim:
Striatal dopamine deficiency is a well-known phenomenon in Dementia with Lewy Bodies (DLB) and can be quantified in vivo by 123I-FP-CIT SPECT (DaTSCAN®). DLB is further characterized by metabolic decline in distinct brain regions as assessible by 18F-FDG-PET. However, the role of striatal glucose metabolism and its linkage to dopamine deficiency in the pathophysiological course of DLB is not sufficiently understood yet. Hence, we made use of the hitherto largest dataset of combined DaTSCAN® and FDG-PET data in DLB deriving from the European DLB consortium (E-DLB) to elucidate the striatal glucose metabolism during disease progression.
Methodik/Methods:
We analysed 162 DLB patients of the European DLB consortium which all had an available FDG-PET and 68 had an available DaTSCAN®. Striatal glucose metabolism normalized by global mean was analyzed as a function of disease duration. Dopamine deficiency was correlated with metabolic changes in the striatum. Finally, we used the striatal quantification of FDG-PET and DaTSCAN® for a voxel-based correlation analysis with FDG-PET to study dopamine-metabolic and metabolic-metabolic connectivity. All data were controlled for center, age, gender, and educational level.
Ergebnisse/Results:
Striatal glucose metabolism increased with disease duration in DLB (R = 0.19, p = 0.02). We observed a strong association of dopamine deficiency with increased glucose metabolism in the striatum (R = 0.55, p < 0.001). Striatal dopamine deficiency and increased striatal glucose metabolism showed similar negative connectivity with parietal and occipital cortical areas and positive connectivity with the limbic system.
Schlussfolgerungen/Conclusions:
Combined analysis of metabolic changes and dopamine deficiency in DLB indicates a strong interrelation of both biomarkers. Increased striatal metabolism may act as a compensatory function of dopamine deficiency and connectivity analyses of subcortical and cortical systems will allow further insight in the pathophysiology of DLB.
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