Changes of dopamine turnover in the progression of Parkinson's disease as measured by positron emission tomography: Their relation to disease-compensatory mechanisms
Identifieur interne : 002D44 ( Main/Exploration ); précédent : 002D43; suivant : 002D45Changes of dopamine turnover in the progression of Parkinson's disease as measured by positron emission tomography: Their relation to disease-compensatory mechanisms
Auteurs : Vesna Sossi [Canada] ; Raul De La Fuente-Fernandez [Canada] ; James E. Holden [Canada] ; Michael Schulzer [Canada] ; Thomas J. Ruth [États-Unis] ; Jon Stoessl [Canada]Source :
- Journal of cerebral blood flow and metabolism [ 0271-678X ] ; 2004.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Brain (diagnostic imaging), Brain (metabolism), Cerebrovascular disease, Dihydroxyphenylalanine (analogs & derivatives), Disease Progression, Dopamine, Dopamine (metabolism), Emission tomography, Female, Fluorine Radioisotopes, Humans, Male, Middle Aged, Nervous system diseases, Parkinson Disease (diagnostic imaging), Parkinson Disease (metabolism), Parkinson disease, Tomography, Emission-Computed, Turnover.
- MESH :
- chemical , analogs & derivatives : Dihydroxyphenylalanine.
- diagnostic imaging : Brain, Parkinson Disease.
- metabolism : Brain, Dopamine, Parkinson Disease.
- Disease Progression, Female, Fluorine Radioisotopes, Humans, Male, Middle Aged, Tomography, Emission-Computed.
Abstract
An increase in dopamine turnover has been shown to occur early in Parkinson's disease (PD). This study investigated changes of dopamine turnover as a function of PD duration using the effective distribution volume (EDV) for dopamine, determined by positron emission tomography with 6-[18F]-fluoro-L-dopa, and compared them with changes in dopamine synthesis and storage ability, quantified with the fluorodopa uptake rate constant Ki. Six healthy subjects, 9 early PD patients (PD1), and 13 advanced PD patients (PD2) participated in the study. In the caudate, the Ki and EDV for PD1 were not significantly different from the normal values, whereas in the putamen Ki was 63% of normal and EDV was only 35%. Between PD1 and PD2 the decline in EDV was higher than that for Ki (caudate 44% and putamen 46% for EDV vs. 21% and 34%, respectively, for Ki). Turnover was higher in the caudate than the putamen in controls, whereas the PD patients exhibited the reverse pattern. This comparison of changes in Ki and EDV as a function of disease progression indicates that a relatively slower decrease in dopamine synthesis and a relatively faster increase in turnover in early disease likely act as compensatory mechanisms, and that the clinical onset of PD reflects a global failure of dopaminergic compensatory mechanisms.
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">An increase in dopamine turnover has been shown to occur early in Parkinson's disease (PD). This study investigated changes of dopamine turnover as a function of PD duration using the effective distribution volume (EDV) for dopamine, determined by positron emission tomography with 6-[<sup>18</sup>
F]-fluoro-L-dopa, and compared them with changes in dopamine synthesis and storage ability, quantified with the fluorodopa uptake rate constant K<sub>i</sub>
. Six healthy subjects, 9 early PD patients (PD1), and 13 advanced PD patients (PD2) participated in the study. In the caudate, the K<sub>i</sub>
and EDV for PD1 were not significantly different from the normal values, whereas in the putamen K<sub>i</sub>
was 63% of normal and EDV was only 35%. Between PD1 and PD2 the decline in EDV was higher than that for K<sub>i</sub>
(caudate 44% and putamen 46% for EDV vs. 21% and 34%, respectively, for K<sub>i</sub>
). Turnover was higher in the caudate than the putamen in controls, whereas the PD patients exhibited the reverse pattern. This comparison of changes in K<sub>i</sub>
and EDV as a function of disease progression indicates that a relatively slower decrease in dopamine synthesis and a relatively faster increase in turnover in early disease likely act as compensatory mechanisms, and that the clinical onset of PD reflects a global failure of dopaminergic compensatory mechanisms.</div>
</front>
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