Abstract
BackgroundAccruing positron emission tomography (PET) studies have suggested that dopaminergic functioning and metabolic changes are correlated with cognitive dysfunction in Parkinson’s disease (PD). Yet, the relationship between dopaminergic or cerebral metabolism and different cognitive domains in PD is poorly understood. To address this scarcity, we aimed to investigate the interactions among dopaminergic bindings, metabolic network changes, and the cognitive domains in PD patients.MethodsWe recruited 41 PD patients, including PD patients with no cognitive impairment (PD-NC; n = 21) and those with mild cognitive impairment (PD-MCI; n = 20). All patients underwent clinical evaluations and a schedule of neuropsychological tests and underwent both 11C-N-2-carbomethoxy-3-(4-fluorophenyl)-tropane (11C-CFT) and 18F-fluorodeoxyglucose (18F-FDG) PET imaging.Results11C-CFT imaging revealed a significant positive correlation between executive function and striatal dopamine transporter (DAT) binding at both the voxel and regional levels. Metabolic imaging revealed that executive function correlated with 18F-FDG uptake, mainly in inferior frontal gyrus, putamen, and insula. Further analysis indicated that striatal DAT binding correlated strictly with metabolic activity in the temporal gyrus, medial frontal gyrus, and cingulate gyrus.ConclusionOur findings might promote the understanding of the neurobiological mechanisms underlying cognitive impairment in PD.
Highlights
Cognitive decline is a prevalent comorbidity in Parkinson’s disease (PD), and up to 80% of patients suffer from dementia (PDD) (Hely et al, 2008)
Some positron emission tomography (PET) studies have demonstrated the significant correlation between striatal dopamine transporter (DAT) binding and executive function (Rinne et al, 2000; Nobili et al, 2010; Siepel et al, 2014; Pellecchia et al, 2015; Kim et al, 2019), whereas a recent study found that DAT binding in the caudate was well correlated with memory and visuospatial dysfunction (Chung et al, 2018)
We aimed to investigate the interactions among dopaminergic abnormalities, cerebral metabolism, and the different cognitive domains and gain further insights into the neurobiological mechanisms related to cognitive impairment in PD
Summary
Cognitive decline is a prevalent comorbidity in Parkinson’s disease (PD), and up to 80% of patients suffer from dementia (PDD) (Hely et al, 2008). Some positron emission tomography (PET) studies have demonstrated the significant correlation between striatal dopamine transporter (DAT) binding and executive function (Rinne et al, 2000; Nobili et al, 2010; Siepel et al, 2014; Pellecchia et al, 2015; Kim et al, 2019), whereas a recent study found that DAT binding in the caudate was well correlated with memory and visuospatial dysfunction (Chung et al, 2018). Accruing positron emission tomography (PET) studies have suggested that dopaminergic functioning and metabolic changes are correlated with cognitive dysfunction in Parkinson’s disease (PD). The relationship between dopaminergic or cerebral metabolism and different cognitive domains in PD is poorly understood. To address this scarcity, we aimed to investigate the interactions among dopaminergic bindings, metabolic network changes, and the cognitive domains in PD patients
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