4.5 Article

Cerebral glucose metabolism in idiopathic REM sleep behavior disorder is different from tau-related and α-synuclein-related neurodegenerative disorders: A brain [18F]FDG PET study

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PARKINSONISM & RELATED DISORDERS
卷 64, 期 -, 页码 97-105

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ELSEVIER SCI LTD
DOI: 10.1016/j.parkreldis.2019.03.017

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Idiopathic RBD; Parkinson's disease; Alzheimer's disease; Lewy body dementia; [18F]FDG PET; Neurodegeneration; Cerebral glucose metabolism

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Introduction: Several longitudinal studies revealed that patients affected by idiopathic REM behavior disorder (iRBD) trend to convert to alpha-synucleinopathies at follow-up, although the time and direction of conversion is currently unpredictable. This study aimed at evaluating brain glucose metabolism, measured by [18F]FDG-PET, in patients affected by iRBD and compared to Parkinson's Disease (PD), Lewy Body Dementia (DLB), Alzheimer's Disease (AD), and controls. Methods: Differences in brain [18F]FDG uptake were analyzed using statistical parametric mapping implemented in Matlab R2012b among iRBD, PD, DLB, AD, and controls. Results: Fifty-four iRBD, 28 PD, 10 DLB, 55 AD, and 35 controls were included in this study. iRBD patients presented an altered [18F]FDG uptake, since the increased [18F]FDG uptake in the brainstem and the reduced [18F]FDG uptake in temporal and parietal regions compared to controls. Moreover, iRBD patients showed several differences in [18F]FDG uptake than PD, DLB, or AD groups, with the main differences documented in the comparison with AD patients. Conclusions: This study documented the alteration of brain [18F]FDG uptake in brainstem and cortical areas of iRBD patients compared to controls. Moreover, the cerebral [18F]FDG uptake of iRBD patients resulted different from that presented by AD, further supporting the hypothesis that tau-related neurodegeneration may not induce RBD manifestations. However, brain [18F]FDG uptake of iRBD patients also differed from that of DLB and PD patients. Hence, these findings further support the hypothesis that iRBD may represent a very early stage of alpha-synucleinopathy in which biomarkers changes already occur but not allow the prediction of phenoconversion.

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