Striatal D2 dopamine receptor status in Parkinson's disease: An [18F]dopa and [11C]Raclopride PET study

Dentresangle, Christine; Veyre, Laurent; Bars, Didier Le; Pierre, Christian; Lávenne, F.; Pollak, Pierre; Guerin, Julie B.; Froment, J; Brousolle, E.

doi:10.1002/1531-8257(199911)14:6<1025::aid-mds1020>3.0.co;2-p

Cited by 45 publications

(27 citation statements)

References 30 publications

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“…Moreover, striatal decreases in [ 18 F]dopa uptake correlated with higher [ 11 C]raclopride binding in early de novo PD patients, suggesting that upregulation of D2R may be a compensatory mechanism in response to synaptic dopamine depletion (Sawle, Playford, Brooks, Quinn, & Frackowiak, 1993). However, as the disease progresses this compensatory upregulation may fail and D2R availability decreases back to normal levels or less in comparison to healthy subjects (Antonini, Schwarz, Oertel, Pogarell, & Leenders, 1997;Brooks et al, 1992;Dentresangle et al, 1999). Moreover, long-term downregulation of striatal dopamine D2R binding may be induced by chronic dopaminergic therapy (Antonini et al, 1997).…”

Section: Dopaminergic Systemmentioning

confidence: 99%

Imaging in Parkinson's Disease

Politis

Pagano

Niccolini

2017

International Review of Neurobiology

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Section: Dopaminergic Systemmentioning

confidence: 99%

Imaging in Parkinson's Disease

Politis

Pagano

Niccolini

2017

International Review of Neurobiology

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“…vesicular storage of 18 F-dopamine (see Figure 1). As 18 F-dopa and non-fluorinated levodopa follow the same metabolic pathway, peripheral COMT inhibition boosts 18 F-dopa bioavailability to the brain and increases its striatal uptake and subsequent metabolism in PD patients.…”

mentioning

confidence: 99%

“…As 18 F-dopa and non-fluorinated levodopa follow the same metabolic pathway, peripheral COMT inhibition boosts 18 F-dopa bioavailability to the brain and increases its striatal uptake and subsequent metabolism in PD patients. Several PET studies have been performed to measure the effect of peripheral COMT inhibitor entacapone on striatal uptake of 18 F-dopa.…”

mentioning

confidence: 99%

“…[4][5][6][7] Striatal K i values can be computed by graphical analysis in two main ways. If a plasma input reference function is used, corrected for levels of 18 F-3-OMD, the striatal K i value primarily reflects the rate constant for dopa decarboxylation. Alternatively, if an occipital cortex reference input function is used, the 18 F reference signal reflects occipital levels of both 18 F-dopa and 18 F-3-OMD in equilibrium with plasma.…”

mentioning

confidence: 99%

“…If a plasma input reference function is used, corrected for levels of 18 F-3-OMD, the striatal K i value primarily reflects the rate constant for dopa decarboxylation. Alternatively, if an occipital cortex reference input function is used, the 18 F reference signal reflects occipital levels of both 18 F-dopa and 18 F-3-OMD in equilibrium with plasma. The striatal K i then reflects the product of the rate constant for dopa decarboxylation and the striatal volume of distribution (VD) of 18 F-dopa.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Continuous Dopaminergic Stimulation in Parkinson’s Disease—What Have We Learned from Positron-emission Tomography?

Brooks¹,

Pavese²

2010

US Neurology

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Oral levodopa remains the most effective symptomatic drug for Dopamine-replacement Treatment and Pre-synaptic Dopaminergic FunctionThe COMT inhibitors entacapone and tolcapone increase levodopa bioavailability in the plasma and increase its transport into the brain by AbstractThe hypothesis that pulsatile stimulation of striatal dopamine receptors in Parkinson's disease (PD) induces molecular and physiologic changes in basal ganglia neurons and may contribute to the development of motor complications has led to the design of therapeutic strategies that provide more continuous dopaminergic stimulation. Newer agents and drug-delivery systems such as slow-release preparations, catechol-O-methyltransferase, and monoamine oxidase inhibitor agents, apomorphine, and Duodopa™ infusions represent a significant step towards less pulsatile dopaminergic administration. However, their efficacy in providing steady brain levels of dopaminergic stimulation in the short and longer term has not yet been proved in patients. This article briefly reviews and discusses the findings of published positron emission tomography (PET) studies that support or oppose the value of continuous dopaminergic stimulation in PD. The potential future value of PET for proof of mechanism in this area is also debated.

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Dopaminergic Function and Dopamine Transporter Binding Assessed With Positron Emission Tomography in Parkinson Disease

Ribeiro¹,

Vidailhet²,

Loc’h³

et al. 2002

Arch Neurol

113

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Uptake of (18)F-dopa may be up-regulated in early PD, suggesting a compensatory increase of dopamine synthesis in surviving dopaminergic terminals. Positron emission tomography dopamine transporter ligands and (18)F-dopa give complementary information on the presynaptic status of the nigrostriatal dopaminergic system and might be associated to investigate the efficacy of neuroprotective treatments in PD.

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Striatal D2 dopamine receptor status in Parkinson's disease: An [18F]dopa and [11C]Raclopride PET study

Cited by 45 publications

References 30 publications

Imaging in Parkinson's Disease

Imaging in Parkinson's Disease

Continuous Dopaminergic Stimulation in Parkinson’s Disease—What Have We Learned from Positron-emission Tomography?

Dopaminergic Function and Dopamine Transporter Binding Assessed With Positron Emission Tomography in Parkinson Disease

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