Longitudinal evolution of compensatory changes in striatal dopamine processing in Parkinson's disease.
Identifieur interne : 001641 ( Main/Exploration ); précédent : 001640; suivant : 001642Longitudinal evolution of compensatory changes in striatal dopamine processing in Parkinson's disease.
Auteurs : Ramachandiran Nandhagopal [Canada] ; Lisa Kuramoto ; Michael Schulzer ; Edwin Mak ; Jacqueline Cragg ; Jess Mckenzie ; Siobhan Mccormick ; Thomas J. Ruth ; Vesna Sossi ; Raul De La Fuente-Fernandez ; A Jon StoesslSource :
- Brain : a journal of neurology [ 1460-2156 ] ; 2011.
English descriptors
- KwdEn :
- Adult, Aged, Corpus Striatum (diagnostic imaging), Corpus Striatum (metabolism), Disease Progression, Dopamine (metabolism), Dopamine Plasma Membrane Transport Proteins (metabolism), Female, Follow-Up Studies, Humans, Longitudinal Studies, Male, Middle Aged, Parkinson Disease (diagnostic imaging), Parkinson Disease (metabolism), Radionuclide Imaging.
- MESH :
- chemical , metabolism : Dopamine, Dopamine Plasma Membrane Transport Proteins.
- diagnostic imaging : Corpus Striatum, Parkinson Disease.
- metabolism : Corpus Striatum, Parkinson Disease.
- Adult, Aged, Disease Progression, Female, Follow-Up Studies, Humans, Longitudinal Studies, Male, Middle Aged, Radionuclide Imaging.
Abstract
Parkinson's disease is a relentlessly progressive neurodegenerative disease. Breakdown of compensatory mechanisms influencing putaminal dopamine processing could contribute to the progressive motor symptoms. We studied a cohort of 78 subjects (at baseline) with sporadic Parkinson's disease and 35 healthy controls with multi-tracer positron emission tomography scans to investigate the evolution of adaptive mechanisms influencing striatal dopamine processing in Parkinson's disease progression. Presynaptic dopaminergic integrity was assessed with three radioligands: (i) [(11)C](±)dihydrotetrabenazine, to estimate the density of vesicular monoamine transporter type 2; (ii) [(11)C]d-threo-methylphenidate, to label the dopamine transporter; and (iii) 6-[(18)F]fluoro-L-DOPA, to assess the activity of aromatic amino acid decarboxylase and storage of 6-[(18)F]-fluorodopamine in synaptic vesicles. The subjects with Parkinson's disease and the healthy controls underwent positron emission tomography scans at the initial visit and after 4 and 8 years of follow-up. Non-linear multivariate regression analyses with random effects were utilized to model the longitudinal changes in tracer values in the putamen standardized relative to normal controls. We found evidence for possible upregulation of dopamine synthesis and downregulation of dopamine transporter in the more severely affected putamen in the early stage of Parkinson's disease. The standardized 6-[(18)F]fluoro-L-DOPA and [(11)C]d-threo-methylphenidate values tended to approach [(11)C](±)dihydrotetrabenazine values in the putamen in later stages of disease (i.e. for [(11)C](±)dihydrotetrabenazine values <25% of normal), when the rates of decline in the positron emission tomography measurements were similar for all the markers. Our data suggest that compensatory mechanisms decline as Parkinson's disease progresses. This breakdown of compensatory strategies in the putamen could contribute to the progression of motor symptoms in advanced disease.
DOI: 10.1093/brain/awr233
PubMed: 22075521
Affiliations:
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Ruth</name></author><author><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name></author><author><name sortKey="De La Fuente Fernandez, Raul" sort="De La Fuente Fernandez, Raul" uniqKey="De La Fuente Fernandez R" first="Raul" last="De La Fuente-Fernandez">Raul De La Fuente-Fernandez</name></author><author><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A Jon" last="Stoessl">A Jon Stoessl</name></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="eISSN">1460-2156</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Corpus Striatum (diagnostic imaging)</term><term>Corpus Striatum (metabolism)</term><term>Disease Progression</term><term>Dopamine (metabolism)</term><term>Dopamine Plasma Membrane Transport Proteins (metabolism)</term><term>Female</term><term>Follow-Up Studies</term><term>Humans</term><term>Longitudinal Studies</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (metabolism)</term><term>Radionuclide Imaging</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Dopamine Plasma Membrane Transport Proteins</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Disease Progression</term><term>Female</term><term>Follow-Up Studies</term><term>Humans</term><term>Longitudinal Studies</term><term>Male</term><term>Middle Aged</term><term>Radionuclide Imaging</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease is a relentlessly progressive neurodegenerative disease. Breakdown of compensatory mechanisms influencing putaminal dopamine processing could contribute to the progressive motor symptoms. We studied a cohort of 78 subjects (at baseline) with sporadic Parkinson's disease and 35 healthy controls with multi-tracer positron emission tomography scans to investigate the evolution of adaptive mechanisms influencing striatal dopamine processing in Parkinson's disease progression. Presynaptic dopaminergic integrity was assessed with three radioligands: (i) [(11)C](±)dihydrotetrabenazine, to estimate the density of vesicular monoamine transporter type 2; (ii) [(11)C]d-threo-methylphenidate, to label the dopamine transporter; and (iii) 6-[(18)F]fluoro-L-DOPA, to assess the activity of aromatic amino acid decarboxylase and storage of 6-[(18)F]-fluorodopamine in synaptic vesicles. The subjects with Parkinson's disease and the healthy controls underwent positron emission tomography scans at the initial visit and after 4 and 8 years of follow-up. Non-linear multivariate regression analyses with random effects were utilized to model the longitudinal changes in tracer values in the putamen standardized relative to normal controls. We found evidence for possible upregulation of dopamine synthesis and downregulation of dopamine transporter in the more severely affected putamen in the early stage of Parkinson's disease. The standardized 6-[(18)F]fluoro-L-DOPA and [(11)C]d-threo-methylphenidate values tended to approach [(11)C](±)dihydrotetrabenazine values in the putamen in later stages of disease (i.e. for [(11)C](±)dihydrotetrabenazine values <25% of normal), when the rates of decline in the positron emission tomography measurements were similar for all the markers. Our data suggest that compensatory mechanisms decline as Parkinson's disease progresses. This breakdown of compensatory strategies in the putamen could contribute to the progression of motor symptoms in advanced disease.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Cragg, Jacqueline" sort="Cragg, Jacqueline" uniqKey="Cragg J" first="Jacqueline" last="Cragg">Jacqueline Cragg</name><name sortKey="De La Fuente Fernandez, Raul" sort="De La Fuente Fernandez, Raul" uniqKey="De La Fuente Fernandez R" first="Raul" last="De La Fuente-Fernandez">Raul De La Fuente-Fernandez</name><name sortKey="Kuramoto, Lisa" sort="Kuramoto, Lisa" uniqKey="Kuramoto L" first="Lisa" last="Kuramoto">Lisa Kuramoto</name><name sortKey="Mak, Edwin" sort="Mak, Edwin" uniqKey="Mak E" first="Edwin" last="Mak">Edwin Mak</name><name sortKey="Mccormick, Siobhan" sort="Mccormick, Siobhan" uniqKey="Mccormick S" first="Siobhan" last="Mccormick">Siobhan Mccormick</name><name sortKey="Mckenzie, Jess" sort="Mckenzie, Jess" uniqKey="Mckenzie J" first="Jess" last="Mckenzie">Jess Mckenzie</name><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J" last="Ruth">Thomas J. Ruth</name><name sortKey="Schulzer, Michael" sort="Schulzer, Michael" uniqKey="Schulzer M" first="Michael" last="Schulzer">Michael Schulzer</name><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A Jon" last="Stoessl">A Jon Stoessl</name></noCountry><country name="Canada"><noRegion><name sortKey="Nandhagopal, Ramachandiran" sort="Nandhagopal, Ramachandiran" uniqKey="Nandhagopal R" first="Ramachandiran" last="Nandhagopal">Ramachandiran Nandhagopal</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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