Longitudinal progression of sporadic Parkinson's disease: a multi-tracer positron emission tomography study.
Identifieur interne : 000B32 ( Ncbi/Merge ); précédent : 000B31; suivant : 000B33Longitudinal progression of sporadic Parkinson's disease: a multi-tracer positron emission tomography study.
Auteurs : R. Nandhagopal ; L. Kuramoto ; M. Schulzer ; E. Mak ; J. Cragg ; Chong S. Lee ; J. Mckenzie ; S. Mccormick ; A. Samii ; A. Troiano ; T J Ruth ; V. Sossi ; R. De La Fuente-Fernandez ; Donald B. Calne ; A J StoesslSource :
- Brain : a journal of neurology [ 1460-2156 ] ; 2009.
English descriptors
- KwdEn :
- Adult, Aged, Caudate Nucleus (diagnostic imaging), Caudate Nucleus (metabolism), Caudate Nucleus (pathology), Disease Progression, Female, Humans, Male, Middle Aged, Parkinson Disease (diagnostic imaging), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Patient Dropouts, Positron-Emission Tomography, Putamen (diagnostic imaging), Putamen (metabolism), Putamen (pathology), Radiopharmaceuticals (metabolism), Young Adult.
- MESH :
- chemical , metabolism : Radiopharmaceuticals.
- diagnostic imaging : Caudate Nucleus, Parkinson Disease, Putamen.
- metabolism : Caudate Nucleus, Putamen.
- pathology : Caudate Nucleus, Parkinson Disease, Putamen.
- physiopathology : Parkinson Disease.
- Adult, Aged, Disease Progression, Female, Humans, Male, Middle Aged, Patient Dropouts, Positron-Emission Tomography, Young Adult.
Abstract
Parkinson's disease is a heterogeneous disorder with multiple factors contributing to disease initiation and progression. Using serial, multi-tracer positron emission tomography imaging, we studied a cohort of 78 subjects with sporadic Parkinson's disease to understand the disease course better. Subjects were scanned with radiotracers of presynaptic dopaminergic integrity at baseline and again after 4 and 8 years of follow-up. Non-linear multivariate regression analyses, using random effects, of the form BP(ND)(t) or K(occ)(t) = a*e((-)(bt)(-d)(A) + c, where BP(ND) = tracer binding potential (nondispaceable), K(OCC) = tracer uptake constant a, b, c and d are regression parameters, t is the symptom duration and A is the age at onset, were utilized to model the longitudinal progression of radiotracer binding/uptake. We found that the initial tracer binding/uptake was significantly different in anterior versus posterior striatal subregions, indicating that the degree of denervation at disease onset was different between regions. However, the relative rate of decline in tracer binding/uptake was similar between the striatal subregions. While an antero-posterior gradient of severity was maintained for dopamine synthesis, storage and reuptake, the asymmetry between the more and less affected striatum became less prominent over the disease course. Our study suggests that the mechanisms underlying Parkinson's disease initiation and progression are probably different. Whereas factors responsible for disease initiation affect striatal subregions differently, those factors contributing to disease progression affect all striatal subregions to a similar degree and may therefore reflect non-specific mechanisms such as oxidative stress, inflammation or excitotoxicity.
DOI: 10.1093/brain/awp209
PubMed: 19690093
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pubmed:19690093Le document en format XML
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Mak</name></author><author><name sortKey="Cragg, J" sort="Cragg, J" uniqKey="Cragg J" first="J" last="Cragg">J. Cragg</name></author><author><name sortKey="Lee, Chong S" sort="Lee, Chong S" uniqKey="Lee C" first="Chong S" last="Lee">Chong S. Lee</name></author><author><name sortKey="Mckenzie, J" sort="Mckenzie, J" uniqKey="Mckenzie J" first="J" last="Mckenzie">J. Mckenzie</name></author><author><name sortKey="Mccormick, S" sort="Mccormick, S" uniqKey="Mccormick S" first="S" last="Mccormick">S. Mccormick</name></author><author><name sortKey="Samii, A" sort="Samii, A" uniqKey="Samii A" first="A" last="Samii">A. Samii</name></author><author><name sortKey="Troiano, A" sort="Troiano, A" uniqKey="Troiano A" first="A" last="Troiano">A. Troiano</name></author><author><name sortKey="Ruth, T J" sort="Ruth, T J" uniqKey="Ruth T" first="T J" last="Ruth">T J Ruth</name></author><author><name sortKey="Sossi, V" sort="Sossi, V" uniqKey="Sossi V" first="V" last="Sossi">V. 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Nandhagopal</name><affiliation><nlm:affiliation>Pacific Parkinson's Research Centre, University of British Columbia & Vancouver Coastal Health, Vancouver, BC V6T2B5 Canada.</nlm:affiliation><wicri:noCountry code="subField">BC V6T2B5 Canada</wicri:noCountry></affiliation></author><author><name sortKey="Kuramoto, L" sort="Kuramoto, L" uniqKey="Kuramoto L" first="L" last="Kuramoto">L. Kuramoto</name></author><author><name sortKey="Schulzer, M" sort="Schulzer, M" uniqKey="Schulzer M" first="M" last="Schulzer">M. Schulzer</name></author><author><name sortKey="Mak, E" sort="Mak, E" uniqKey="Mak E" first="E" last="Mak">E. Mak</name></author><author><name sortKey="Cragg, J" sort="Cragg, J" uniqKey="Cragg J" first="J" last="Cragg">J. Cragg</name></author><author><name sortKey="Lee, Chong S" sort="Lee, Chong S" uniqKey="Lee C" first="Chong S" last="Lee">Chong S. Lee</name></author><author><name sortKey="Mckenzie, J" sort="Mckenzie, J" uniqKey="Mckenzie J" first="J" last="Mckenzie">J. Mckenzie</name></author><author><name sortKey="Mccormick, S" sort="Mccormick, S" uniqKey="Mccormick S" first="S" last="Mccormick">S. Mccormick</name></author><author><name sortKey="Samii, A" sort="Samii, A" uniqKey="Samii A" first="A" last="Samii">A. Samii</name></author><author><name sortKey="Troiano, A" sort="Troiano, A" uniqKey="Troiano A" first="A" last="Troiano">A. Troiano</name></author><author><name sortKey="Ruth, T J" sort="Ruth, T J" uniqKey="Ruth T" first="T J" last="Ruth">T J Ruth</name></author><author><name sortKey="Sossi, V" sort="Sossi, V" uniqKey="Sossi V" first="V" last="Sossi">V. Sossi</name></author><author><name sortKey="De La Fuente Fernandez, R" sort="De La Fuente Fernandez, R" uniqKey="De La Fuente Fernandez R" first="R" last="De La Fuente-Fernandez">R. De La Fuente-Fernandez</name></author><author><name sortKey="Calne, Donald B" sort="Calne, Donald B" uniqKey="Calne D" first="Donald B" last="Calne">Donald B. Calne</name></author><author><name sortKey="Stoessl, A J" sort="Stoessl, A J" uniqKey="Stoessl A" first="A J" last="Stoessl">A J Stoessl</name></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="eISSN">1460-2156</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Caudate Nucleus (diagnostic imaging)</term><term>Caudate Nucleus (metabolism)</term><term>Caudate Nucleus (pathology)</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Patient Dropouts</term><term>Positron-Emission Tomography</term><term>Putamen (diagnostic imaging)</term><term>Putamen (metabolism)</term><term>Putamen (pathology)</term><term>Radiopharmaceuticals (metabolism)</term><term>Young Adult</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Radiopharmaceuticals</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Caudate Nucleus</term><term>Parkinson Disease</term><term>Putamen</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Caudate Nucleus</term><term>Putamen</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Caudate Nucleus</term><term>Parkinson Disease</term><term>Putamen</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><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>Humans</term><term>Male</term><term>Middle Aged</term><term>Patient Dropouts</term><term>Positron-Emission Tomography</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease is a heterogeneous disorder with multiple factors contributing to disease initiation and progression. Using serial, multi-tracer positron emission tomography imaging, we studied a cohort of 78 subjects with sporadic Parkinson's disease to understand the disease course better. Subjects were scanned with radiotracers of presynaptic dopaminergic integrity at baseline and again after 4 and 8 years of follow-up. Non-linear multivariate regression analyses, using random effects, of the form BP(ND)(t) or K(occ)(t) = a*e((-)(bt)(-d)(A) + c, where BP(ND) = tracer binding potential (nondispaceable), K(OCC) = tracer uptake constant a, b, c and d are regression parameters, t is the symptom duration and A is the age at onset, were utilized to model the longitudinal progression of radiotracer binding/uptake. We found that the initial tracer binding/uptake was significantly different in anterior versus posterior striatal subregions, indicating that the degree of denervation at disease onset was different between regions. However, the relative rate of decline in tracer binding/uptake was similar between the striatal subregions. While an antero-posterior gradient of severity was maintained for dopamine synthesis, storage and reuptake, the asymmetry between the more and less affected striatum became less prominent over the disease course. Our study suggests that the mechanisms underlying Parkinson's disease initiation and progression are probably different. Whereas factors responsible for disease initiation affect striatal subregions differently, those factors contributing to disease progression affect all striatal subregions to a similar degree and may therefore reflect non-specific mechanisms such as oxidative stress, inflammation or excitotoxicity.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19690093</PMID><DateCreated><Year>2009</Year><Month>10</Month><Day>28</Day></DateCreated><DateCompleted><Year>2010</Year><Month>01</Month><Day>15</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2156</ISSN><JournalIssue CitedMedium="Internet"><Volume>132</Volume><Issue>Pt 11</Issue><PubDate><Year>2009</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Longitudinal progression of sporadic Parkinson's disease: a multi-tracer positron emission tomography study.</ArticleTitle><Pagination><MedlinePgn>2970-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/brain/awp209</ELocationID><Abstract><AbstractText>Parkinson's disease is a heterogeneous disorder with multiple factors contributing to disease initiation and progression. Using serial, multi-tracer positron emission tomography imaging, we studied a cohort of 78 subjects with sporadic Parkinson's disease to understand the disease course better. Subjects were scanned with radiotracers of presynaptic dopaminergic integrity at baseline and again after 4 and 8 years of follow-up. Non-linear multivariate regression analyses, using random effects, of the form BP(ND)(t) or K(occ)(t) = a*e((-)(bt)(-d)(A) + c, where BP(ND) = tracer binding potential (nondispaceable), K(OCC) = tracer uptake constant a, b, c and d are regression parameters, t is the symptom duration and A is the age at onset, were utilized to model the longitudinal progression of radiotracer binding/uptake. We found that the initial tracer binding/uptake was significantly different in anterior versus posterior striatal subregions, indicating that the degree of denervation at disease onset was different between regions. However, the relative rate of decline in tracer binding/uptake was similar between the striatal subregions. While an antero-posterior gradient of severity was maintained for dopamine synthesis, storage and reuptake, the asymmetry between the more and less affected striatum became less prominent over the disease course. Our study suggests that the mechanisms underlying Parkinson's disease initiation and progression are probably different. Whereas factors responsible for disease initiation affect striatal subregions differently, those factors contributing to disease progression affect all striatal subregions to a similar degree and may therefore reflect non-specific mechanisms such as oxidative stress, inflammation or excitotoxicity.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nandhagopal</LastName><ForeName>R</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Pacific Parkinson's Research Centre, University of British Columbia & Vancouver Coastal Health, Vancouver, BC V6T2B5 Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kuramoto</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Schulzer</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Mak</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Cragg</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Chong S</ForeName><Initials>CS</Initials></Author><Author ValidYN="Y"><LastName>McKenzie</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>McCormick</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Samii</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Troiano</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Ruth</LastName><ForeName>T J</ForeName><Initials>TJ</Initials></Author><Author ValidYN="Y"><LastName>Sossi</LastName><ForeName>V</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>de la Fuente-Fernandez</LastName><ForeName>R</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Calne</LastName><ForeName>Donald B</ForeName><Initials>DB</Initials></Author><Author ValidYN="Y"><LastName>Stoessl</LastName><ForeName>A J</ForeName><Initials>AJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>08</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019275">Radiopharmaceuticals</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002421" MajorTopicYN="N">Caudate Nucleus</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="Y">Parkinson Disease</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010352" MajorTopicYN="N">Patient Dropouts</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049268" MajorTopicYN="N">Positron-Emission Tomography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011699" MajorTopicYN="N">Putamen</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019275" MajorTopicYN="N">Radiopharmaceuticals</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>8</Month><Day>20</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>8</Month><Day>20</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>1</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19690093</ArticleId><ArticleId IdType="pii">awp209</ArticleId><ArticleId IdType="doi">10.1093/brain/awp209</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Calne, Donald B" sort="Calne, Donald B" uniqKey="Calne D" first="Donald B" last="Calne">Donald B. Calne</name><name sortKey="Cragg, J" sort="Cragg, J" uniqKey="Cragg J" first="J" last="Cragg">J. Cragg</name><name sortKey="De La Fuente Fernandez, R" sort="De La Fuente Fernandez, R" uniqKey="De La Fuente Fernandez R" first="R" last="De La Fuente-Fernandez">R. De La Fuente-Fernandez</name><name sortKey="Kuramoto, L" sort="Kuramoto, L" uniqKey="Kuramoto L" first="L" last="Kuramoto">L. Kuramoto</name><name sortKey="Lee, Chong S" sort="Lee, Chong S" uniqKey="Lee C" first="Chong S" last="Lee">Chong S. Lee</name><name sortKey="Mak, E" sort="Mak, E" uniqKey="Mak E" first="E" last="Mak">E. Mak</name><name sortKey="Mccormick, S" sort="Mccormick, S" uniqKey="Mccormick S" first="S" last="Mccormick">S. Mccormick</name><name sortKey="Mckenzie, J" sort="Mckenzie, J" uniqKey="Mckenzie J" first="J" last="Mckenzie">J. Mckenzie</name><name sortKey="Nandhagopal, R" sort="Nandhagopal, R" uniqKey="Nandhagopal R" first="R" last="Nandhagopal">R. Nandhagopal</name><name sortKey="Ruth, T J" sort="Ruth, T J" uniqKey="Ruth T" first="T J" last="Ruth">T J Ruth</name><name sortKey="Samii, A" sort="Samii, A" uniqKey="Samii A" first="A" last="Samii">A. Samii</name><name sortKey="Schulzer, M" sort="Schulzer, M" uniqKey="Schulzer M" first="M" last="Schulzer">M. Schulzer</name><name sortKey="Sossi, V" sort="Sossi, V" uniqKey="Sossi V" first="V" last="Sossi">V. Sossi</name><name sortKey="Stoessl, A J" sort="Stoessl, A J" uniqKey="Stoessl A" first="A J" last="Stoessl">A J Stoessl</name><name sortKey="Troiano, A" sort="Troiano, A" uniqKey="Troiano A" first="A" last="Troiano">A. Troiano</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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