Antineuronal antibodies in Parkinson's disease.
Identifieur interne : 002090 ( Ncbi/Merge ); précédent : 002089; suivant : 002091Antineuronal antibodies in Parkinson's disease.
Auteurs : Bart P C. Van De Warrenburg [Royaume-Uni] ; Andrew J. Church ; Davide Martino ; Paul M. Candler ; Kailash P. Bhatia ; Gavin Giovannoni ; Niall P. QuinnSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- Antibodies (immunology), Antigens (immunology), Basal Ganglia (immunology), Basal Ganglia (pathology), Blotting, Western, Carrier Proteins (metabolism), Cerebellum (enzymology), Cerebellum (immunology), Cerebellum (pathology), Female, Humans, Inflammation (complications), Inflammation (immunology), Inflammation (pathology), Male, Membrane Proteins (metabolism), Middle Aged, Neurons (immunology), Neurons (metabolism), Neurons (pathology), Parkinson Disease (complications), Parkinson Disease (immunology), Parkinson Disease (pathology), Phosphopyruvate Hydratase (metabolism), Reverse Transcriptase Polymerase Chain Reaction, Thyroid Hormones (metabolism).
- MESH :
- chemical , immunology : Antibodies, Antigens.
- complications : Inflammation, Parkinson Disease.
- enzymology : Cerebellum.
- immunology : Basal Ganglia, Cerebellum, Inflammation, Neurons, Parkinson Disease.
- chemical , metabolism : Carrier Proteins, Membrane Proteins, Neurons, Phosphopyruvate Hydratase, Thyroid Hormones.
- pathology : Basal Ganglia, Cerebellum, Inflammation, Neurons, Parkinson Disease.
- Blotting, Western, Female, Humans, Male, Middle Aged, Reverse Transcriptase Polymerase Chain Reaction.
Abstract
Antineuronal antibodies (ANAs) have been implicated in the pathophysiology of postinfectious movement disorders, such as Sydenham's chorea. However, their relevance in other movement disorders--in the absence of infectious triggers--remains much disputed. We sought to assess the frequency of ANAs in idiopathic Parkinson's disease (IPD) and to explore whether a specific phenotype is associated with the presence of ANAs. For this purpose, we recruited 76 IPD patients, 9 patients with genetic parkinsonism, and 10 with one of the parkinson-plus syndromes. They were all subjected to a comprehensive clinical review. In addition, 50 patients with non-extrapyramidal neurological disease and 30 healthy blood donors served as control populations. Blood samples were tested for the presence of ANAs with Western blotting, using recombinant proteins of the three putative antigens (aldolase C, neuron-specific enolase, and pyruvate kinase M1). We found these antibodies in 11.8% of the 76 IPD patients, which differed significantly from healthy controls (0%, P = 0.043), but nonsignificantly from patients with genetic parkinsonism (11.1%), with a parkinson-plus syndrome (10%), or from neurological disease controls (4%). With respect to relevant disease characteristics, IPD patients with or without ANAs were indistinguishable, except for atypical disease features (mainly early falls or freezing and marked Pisa syndrome), which were more frequent in the ANA-positive IPD group. We conclude that ANAs do not play a role in the majority of patients with IPD, but might be relevant in the pathogenesis of IPD with atypical features.
DOI: 10.1002/mds.21929
PubMed: 18383532
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Van De Warrenburg</name><affiliation wicri:level="3"><nlm:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, United Kingdom. b.vandewarrenburg@neuro.umcn.nl</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Church, Andrew J" sort="Church, Andrew J" uniqKey="Church A" first="Andrew J" last="Church">Andrew J. Church</name></author><author><name sortKey="Martino, Davide" sort="Martino, Davide" uniqKey="Martino D" first="Davide" last="Martino">Davide Martino</name></author><author><name sortKey="Candler, Paul M" sort="Candler, Paul M" uniqKey="Candler P" first="Paul M" last="Candler">Paul M. Candler</name></author><author><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P" last="Bhatia">Kailash P. Bhatia</name></author><author><name sortKey="Giovannoni, Gavin" sort="Giovannoni, Gavin" uniqKey="Giovannoni G" first="Gavin" last="Giovannoni">Gavin Giovannoni</name></author><author><name sortKey="Quinn, Niall P" sort="Quinn, Niall P" uniqKey="Quinn N" first="Niall P" last="Quinn">Niall P. 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Van De Warrenburg</name><affiliation wicri:level="3"><nlm:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, United Kingdom. b.vandewarrenburg@neuro.umcn.nl</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Church, Andrew J" sort="Church, Andrew J" uniqKey="Church A" first="Andrew J" last="Church">Andrew J. Church</name></author><author><name sortKey="Martino, Davide" sort="Martino, Davide" uniqKey="Martino D" first="Davide" last="Martino">Davide Martino</name></author><author><name sortKey="Candler, Paul M" sort="Candler, Paul M" uniqKey="Candler P" first="Paul M" last="Candler">Paul M. Candler</name></author><author><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P" last="Bhatia">Kailash P. Bhatia</name></author><author><name sortKey="Giovannoni, Gavin" sort="Giovannoni, Gavin" uniqKey="Giovannoni G" first="Gavin" last="Giovannoni">Gavin Giovannoni</name></author><author><name sortKey="Quinn, Niall P" sort="Quinn, Niall P" uniqKey="Quinn N" first="Niall P" last="Quinn">Niall P. Quinn</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antibodies (immunology)</term><term>Antigens (immunology)</term><term>Basal Ganglia (immunology)</term><term>Basal Ganglia (pathology)</term><term>Blotting, Western</term><term>Carrier Proteins (metabolism)</term><term>Cerebellum (enzymology)</term><term>Cerebellum (immunology)</term><term>Cerebellum (pathology)</term><term>Female</term><term>Humans</term><term>Inflammation (complications)</term><term>Inflammation (immunology)</term><term>Inflammation (pathology)</term><term>Male</term><term>Membrane Proteins (metabolism)</term><term>Middle Aged</term><term>Neurons (immunology)</term><term>Neurons (metabolism)</term><term>Neurons (pathology)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (immunology)</term><term>Parkinson Disease (pathology)</term><term>Phosphopyruvate Hydratase (metabolism)</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Thyroid Hormones (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antibodies</term><term>Antigens</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Inflammation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Cerebellum</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Basal Ganglia</term><term>Cerebellum</term><term>Inflammation</term><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carrier Proteins</term><term>Membrane Proteins</term><term>Neurons</term><term>Phosphopyruvate Hydratase</term><term>Thyroid Hormones</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term><term>Cerebellum</term><term>Inflammation</term><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Blotting, Western</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Reverse Transcriptase Polymerase Chain Reaction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Antineuronal antibodies (ANAs) have been implicated in the pathophysiology of postinfectious movement disorders, such as Sydenham's chorea. However, their relevance in other movement disorders--in the absence of infectious triggers--remains much disputed. We sought to assess the frequency of ANAs in idiopathic Parkinson's disease (IPD) and to explore whether a specific phenotype is associated with the presence of ANAs. For this purpose, we recruited 76 IPD patients, 9 patients with genetic parkinsonism, and 10 with one of the parkinson-plus syndromes. They were all subjected to a comprehensive clinical review. In addition, 50 patients with non-extrapyramidal neurological disease and 30 healthy blood donors served as control populations. Blood samples were tested for the presence of ANAs with Western blotting, using recombinant proteins of the three putative antigens (aldolase C, neuron-specific enolase, and pyruvate kinase M1). We found these antibodies in 11.8% of the 76 IPD patients, which differed significantly from healthy controls (0%, P = 0.043), but nonsignificantly from patients with genetic parkinsonism (11.1%), with a parkinson-plus syndrome (10%), or from neurological disease controls (4%). With respect to relevant disease characteristics, IPD patients with or without ANAs were indistinguishable, except for atypical disease features (mainly early falls or freezing and marked Pisa syndrome), which were more frequent in the ANA-positive IPD group. We conclude that ANAs do not play a role in the majority of patients with IPD, but might be relevant in the pathogenesis of IPD with atypical features.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">18383532</PMID><DateCreated><Year>2008</Year><Month>06</Month><Day>03</Day></DateCreated><DateCompleted><Year>2008</Year><Month>08</Month><Day>14</Day></DateCompleted><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>7</Issue><PubDate><Year>2008</Year><Month>May</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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In addition, 50 patients with non-extrapyramidal neurological disease and 30 healthy blood donors served as control populations. Blood samples were tested for the presence of ANAs with Western blotting, using recombinant proteins of the three putative antigens (aldolase C, neuron-specific enolase, and pyruvate kinase M1). We found these antibodies in 11.8% of the 76 IPD patients, which differed significantly from healthy controls (0%, P = 0.043), but nonsignificantly from patients with genetic parkinsonism (11.1%), with a parkinson-plus syndrome (10%), or from neurological disease controls (4%). With respect to relevant disease characteristics, IPD patients with or without ANAs were indistinguishable, except for atypical disease features (mainly early falls or freezing and marked Pisa syndrome), which were more frequent in the ANA-positive IPD group. We conclude that ANAs do not play a role in the majority of patients with IPD, but might be relevant in the pathogenesis of IPD with atypical features.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>van de Warrenburg</LastName><ForeName>Bart P C</ForeName><Initials>BP</Initials><AffiliationInfo><Affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, United Kingdom. b.vandewarrenburg@neuro.umcn.nl</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Church</LastName><ForeName>Andrew J</ForeName><Initials>AJ</Initials></Author><Author ValidYN="Y"><LastName>Martino</LastName><ForeName>Davide</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Candler</LastName><ForeName>Paul M</ForeName><Initials>PM</Initials></Author><Author ValidYN="Y"><LastName>Bhatia</LastName><ForeName>Kailash P</ForeName><Initials>KP</Initials></Author><Author ValidYN="Y"><LastName>Giovannoni</LastName><ForeName>Gavin</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Quinn</LastName><ForeName>Niall P</ForeName><Initials>NP</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000906">Antibodies</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000941">Antigens</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013963">Thyroid Hormones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C053648">thyroid hormone-binding proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 4.2.1.11</RegistryNumber><NameOfSubstance UI="D010751">Phosphopyruvate Hydratase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000906">Antibodies</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000276">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000941">Antigens</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000276">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001479">Basal Ganglia</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000276">immunology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015153">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002352">Carrier Proteins</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002531">Cerebellum</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000201">enzymology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000276">immunology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007249">Inflammation</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000276">immunology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008565">Membrane Proteins</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009474">Neurons</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000276">immunology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="N" UI="Q000276">immunology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010751">Phosphopyruvate Hydratase</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020133">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013963">Thyroid Hormones</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>4</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>8</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>4</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.21929</ArticleId><ArticleId IdType="pubmed">18383532</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><noCountry><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P" last="Bhatia">Kailash P. Bhatia</name><name sortKey="Candler, Paul M" sort="Candler, Paul M" uniqKey="Candler P" first="Paul M" last="Candler">Paul M. Candler</name><name sortKey="Church, Andrew J" sort="Church, Andrew J" uniqKey="Church A" first="Andrew J" last="Church">Andrew J. Church</name><name sortKey="Giovannoni, Gavin" sort="Giovannoni, Gavin" uniqKey="Giovannoni G" first="Gavin" last="Giovannoni">Gavin Giovannoni</name><name sortKey="Martino, Davide" sort="Martino, Davide" uniqKey="Martino D" first="Davide" last="Martino">Davide Martino</name><name sortKey="Quinn, Niall P" sort="Quinn, Niall P" uniqKey="Quinn N" first="Niall P" last="Quinn">Niall P. Quinn</name></noCountry><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Van De Warrenburg, Bart P C" sort="Van De Warrenburg, Bart P C" uniqKey="Van De Warrenburg B" first="Bart P C" last="Van De Warrenburg">Bart P C. Van De Warrenburg</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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