Interaction of caudate dopamine depletion and brain metabolic changes with cognitive dysfunction in early Parkinson's disease

Polito, Cristina; Berti, Valentina; Ramat, Silvia; Vanzi, E.; Cristofaro, Maria Teresa De; Pellicanò, Giannantonio; Mungai, Francesco; Marini, P.; Formiconi, Andreas Robert; Sorbi, Sandro; Pupi, Alberto

doi:10.1016/j.neurobiolaging.2010.09.004

Cited by 79 publications

(64 citation statements)

References 61 publications

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“…5). These findings were compatible with the reports of other functional imaging studies that demonstrated a significantly functional disruption of frontostriatal circuits in early and nondementic PD (44,45). Our results suggested the usefulness of 18 F-DTBZ PET in measuring the distribution of VMAT2 density in the mesolimbic system.…”

Section: Disscussionsupporting

confidence: 93%

In Vivo Detection of Monoaminergic Degeneration in Early Parkinson Disease by ¹⁸F-9-Fluoropropyl-(+)-Dihydrotetrabenzazine PET

Lin

Hsiao

et al. 2013

J Nucl Med

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PET with 18 F-9-fluoropropyl-(1)-dihydrotetrabenzazine ( 18 F-DTBZ), a novel radiotracer targeting vesicular monoamine transporter type 2 (VMAT2), has been proven as a useful imaging marker to measure dopaminergic integrity. Methods: The aim of this study was to evaluate the capability of 18 F-DTBZ PET in detecting the monoaminergic degeneration in early Parkinson disease (PD) in vivo. Seventeen age-matched healthy subjects and 30 PD patients at early stage of disease (duration of disease # 5 y) with mild and unilateral motor symptoms underwent 18 F-DTBZ PET scans. The severity of disease, including Unified Parkinson Disease Rating Scale and modified Hoehn and Yahr Stage (mHY), were recorded at off-medication states. The standardized volumes of interest were applied to the spatial normalized image for quantification analysis. The specific uptake ratios (SURs) were calculated according to the formula (specific volumes-of-interest counts/occipital cortex counts) 2 1. SUR measurements were summarized for each brain region. Results: The mean duration of disease in the PD group was 3.2 6 2.1 y (range, 0.5-5 y). The mean mHY was 1.0 6 0.1 (range, 1-1.5). The SURs of bilateral caudate, anterior putamen, posterior putamen, substantia nigra, and nucleus accumbens were significantly lower in PD patients than those of healthy subjects. The reduction of SURs was most severe in the contralateral (the brain regions that are located opposite to the symptomatic side) posterior putamen (281%), followed by the ipsilateral posterior putamen (267%). Receiver-operating-characteristic curve analysis showed that the SURs of the bilateral posterior putamen and contralateral anterior putamen had a sensitivity of 100% and specificity of 100% in differentiating PD patients from healthy subjects. Conclusion: 18 F-DTBZ PET was as an excellent tool for the early diagnosis of PD. The obvious decline of 18 F-DTBZ uptake in the ipsilateral (asymptomatic) striatum suggested that 18 F-DTBZ PET might serve as an in vivo biomarker to detect the monoaminergic degeneration in the premotor phase of PD.

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Section: Disscussionsupporting

confidence: 93%

In Vivo Detection of Monoaminergic Degeneration in Early Parkinson Disease by ¹⁸F-9-Fluoropropyl-(+)-Dihydrotetrabenzazine PET

Lin

Hsiao

et al. 2013

J Nucl Med

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“…In agreement with that, we show in the present study that PDMCI + under-recruited bilateral medial prefrontal cortex (including ACC) compared to PDMCI − , and that the alterations persist across time. ACC is related to high-level cognitive processing (Duncan and Owen, 2000), and PD-related alterations are associated with striatal dopaminergic depletions (Ito et al, 2002), decreased metabolism (Polito et al, 2012), and loss of neuronal integrity (Lewis et al, 2012). …”

Section: Discussionmentioning

confidence: 99%

Longitudinal changes in task-evoked brain responses in Parkinson's disease patients with and without mild cognitive impairment

et al. 2014

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Cognitive deficits are common in Parkinson's disease. Previous cross-sectional research has demonstrated a link between cognitive impairments and fronto-striatal dopaminergic dysmodulation. However, longitudinal studies that link disease progression with altered task-evoked brain activity are lacking. Therefore, our objective was to longitudinally evaluate working-memory related brain activity changes in Parkinson's disease patients with and without mild cognitive impairment (MCI). Patients were recruited within a longitudinal cohort study of incident patients with idiopathic parkinsonism. We longitudinally (at baseline examination and at 12-months follow-up) compared 28 patients with Parkinson's disease without MCI with 11 patients with Parkinson's disease and MCI. Functional MRI blood oxygen level dependent signal was measured during a verbal two-back working-memory task. Patients with MCI under-recruited bilateral medial prefrontal cortex at both time-points (main effect of group: p < 0.001, uncorrected). Critically, a significant group-by-time interaction effect (p < 0.001, uncorrected) was found in the right fusiform gyrus, indicating that working-memory related activity decreased for patients with Parkinson's disease and MCI between baseline and follow-up, while patients without MCI were stable across time-points. The functional connectivity between right fusiform gyrus and bilateral caudate nucleus was stronger for patients without MCI relative to patients with MCI. Our findings support the view that deficits in working-memory updating are related to persistent fronto-striatal under-recruitments in patients with early phase Parkinson's disease and MCI. The longitudinal evolution of MCI in Parkinson's disease translates into additional task-evoked posterior cortical changes.

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“…Additionally, the long-range FCD reductions mainly involve the middle and superior frontal gyrus, where significant reductions in the cerebral blood flow, cerebral glucose metabolism and gray matter volume and thickness have also been documented in PD patients [5,31,32,34]. In PD patients, several studies have implicated a dysfunctional frontostriatal circuit in the pathophysiology of the cognitive dysfunction in PD [35,36]. Because our previous study detected significant volumetric atrophy in the caudate nucleus [10], the observed long-range FCD reductions in the middle and superior frontal gyrus might be caused by abnormal frontostriatal connectivity in PD patients and might be related to the cognitive dysfunction of PD patients.…”

Section: Decreased Short-and Long-range Fcds In Pd Patientsmentioning

confidence: 99%

Abnormal functional connectivity density in Parkinson's disease

Zhang

et al. 2015

Behavioural Brain Research

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Interaction of caudate dopamine depletion and brain metabolic changes with cognitive dysfunction in early Parkinson's disease

Cited by 79 publications

References 61 publications

In Vivo Detection of Monoaminergic Degeneration in Early Parkinson Disease by ¹⁸F-9-Fluoropropyl-(+)-Dihydrotetrabenzazine PET

In Vivo Detection of Monoaminergic Degeneration in Early Parkinson Disease by ¹⁸F-9-Fluoropropyl-(+)-Dihydrotetrabenzazine PET

Longitudinal changes in task-evoked brain responses in Parkinson's disease patients with and without mild cognitive impairment

Abnormal functional connectivity density in Parkinson's disease

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Interaction of caudate dopamine depletion and brain metabolic changes with cognitive dysfunction in early Parkinson's disease

Cited by 79 publications

References 61 publications

In Vivo Detection of Monoaminergic Degeneration in Early Parkinson Disease by 18F-9-Fluoropropyl-(+)-Dihydrotetrabenzazine PET

In Vivo Detection of Monoaminergic Degeneration in Early Parkinson Disease by 18F-9-Fluoropropyl-(+)-Dihydrotetrabenzazine PET

Longitudinal changes in task-evoked brain responses in Parkinson's disease patients with and without mild cognitive impairment

Abnormal functional connectivity density in Parkinson's disease

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Product

Resources

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In Vivo Detection of Monoaminergic Degeneration in Early Parkinson Disease by ¹⁸F-9-Fluoropropyl-(+)-Dihydrotetrabenzazine PET

In Vivo Detection of Monoaminergic Degeneration in Early Parkinson Disease by ¹⁸F-9-Fluoropropyl-(+)-Dihydrotetrabenzazine PET