Antineuronal Antibodies in Parkinson's Disease
Identifieur interne : 001238 ( PascalFrancis/Corpus ); précédent : 001237; suivant : 001239Antineuronal Antibodies in Parkinson's Disease
Auteurs : Bart P. C. Van De Warrenburg ; Andrew J. Church ; Davide Martino ; Paul M. Candler ; Kailash P. Bhatia ; Gavin Giovannoni ; Niall P. QuinnSource :
- Movement disorders [ 0885-3185 ] ; 2008.
Descripteurs français
- Pascal (Inist)
English descriptors
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 Ml). 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.
Notice en format standard (ISO 2709)
Pour connaître la documentation sur le format Inist Standard.
pA |
|
---|
Format Inist (serveur)
NO : | PASCAL 08-0305144 INIST |
---|---|
ET : | Antineuronal Antibodies in Parkinson's Disease |
AU : | VAN DE WARRENBURG (Bart P. C.); CHURCH (Andrew J.); MARTINO (Davide); CANDLER (Paul M.); BHATIA (Kailash P.); GIOVANNONI (Gavin); QUINN (Niall P.) |
AF : | Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology/London/Royaume-Uni (1 aut., 3 aut., 5 aut., 7 aut.); Department of Neurology, Radboud University Nijmegen Medical Centre/Nijmegen/Pays-Bas (1 aut.); Department of Neuroimmunology, Institute of Neurology/London/Royaume-Uni (2 aut., 3 aut., 4 aut.); Department of Neurological and Psychiatric Sciences, University of Bari/Bari/Italie (3 aut.); Institute of Cell and Molecular Science, Queen Mary University London and the Department of Neurology, Barts and The London NHS Trust/London/Royaume-Uni (6 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2008; Vol. 23; No. 7; Pp. 958-963; Bibl. 22 ref. |
LA : | Anglais |
EA : | 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 Ml). 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. |
CC : | 002B17; 002B17G |
FD : | Maladie de Parkinson; Pathologie du système nerveux; Inflammation |
FG : | Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central |
ED : | Parkinson disease; Nervous system diseases; Inflammation |
EG : | Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease |
SD : | Parkinson enfermedad; Sistema nervioso patología; Inflamación |
LO : | INIST-20953.354000200276040050 |
ID : | 08-0305144 |
Links to Exploration step
Pascal:08-0305144Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Antineuronal Antibodies in Parkinson's Disease</title>
<author><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>
<affiliation><inist:fA14 i1="01"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Department of Neurology, Radboud University Nijmegen Medical Centre</s1>
<s2>Nijmegen</s2>
<s3>NLD</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Church, Andrew J" sort="Church, Andrew J" uniqKey="Church A" first="Andrew J." last="Church">Andrew J. Church</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Neuroimmunology, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Martino, Davide" sort="Martino, Davide" uniqKey="Martino D" first="Davide" last="Martino">Davide Martino</name>
<affiliation><inist:fA14 i1="01"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="03"><s1>Department of Neuroimmunology, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="04"><s1>Department of Neurological and Psychiatric Sciences, University of Bari</s1>
<s2>Bari</s2>
<s3>ITA</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Candler, Paul M" sort="Candler, Paul M" uniqKey="Candler P" first="Paul M." last="Candler">Paul M. Candler</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Neuroimmunology, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P." last="Bhatia">Kailash P. Bhatia</name>
<affiliation><inist:fA14 i1="01"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Giovannoni, Gavin" sort="Giovannoni, Gavin" uniqKey="Giovannoni G" first="Gavin" last="Giovannoni">Gavin Giovannoni</name>
<affiliation><inist:fA14 i1="05"><s1>Institute of Cell and Molecular Science, Queen Mary University London and the Department of Neurology, Barts and The London NHS Trust</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Quinn, Niall P" sort="Quinn, Niall P" uniqKey="Quinn N" first="Niall P." last="Quinn">Niall P. Quinn</name>
<affiliation><inist:fA14 i1="01"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">08-0305144</idno>
<date when="2008">2008</date>
<idno type="stanalyst">PASCAL 08-0305144 INIST</idno>
<idno type="RBID">Pascal:08-0305144</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">001238</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Antineuronal Antibodies in Parkinson's Disease</title>
<author><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>
<affiliation><inist:fA14 i1="01"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Department of Neurology, Radboud University Nijmegen Medical Centre</s1>
<s2>Nijmegen</s2>
<s3>NLD</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Church, Andrew J" sort="Church, Andrew J" uniqKey="Church A" first="Andrew J." last="Church">Andrew J. Church</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Neuroimmunology, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Martino, Davide" sort="Martino, Davide" uniqKey="Martino D" first="Davide" last="Martino">Davide Martino</name>
<affiliation><inist:fA14 i1="01"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="03"><s1>Department of Neuroimmunology, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="04"><s1>Department of Neurological and Psychiatric Sciences, University of Bari</s1>
<s2>Bari</s2>
<s3>ITA</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Candler, Paul M" sort="Candler, Paul M" uniqKey="Candler P" first="Paul M." last="Candler">Paul M. Candler</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Neuroimmunology, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P." last="Bhatia">Kailash P. Bhatia</name>
<affiliation><inist:fA14 i1="01"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Giovannoni, Gavin" sort="Giovannoni, Gavin" uniqKey="Giovannoni G" first="Gavin" last="Giovannoni">Gavin Giovannoni</name>
<affiliation><inist:fA14 i1="05"><s1>Institute of Cell and Molecular Science, Queen Mary University London and the Department of Neurology, Barts and The London NHS Trust</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Quinn, Niall P" sort="Quinn, Niall P" uniqKey="Quinn N" first="Niall P." last="Quinn">Niall P. Quinn</name>
<affiliation><inist:fA14 i1="01"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
<imprint><date when="2008">2008</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Inflammation</term>
<term>Nervous system diseases</term>
<term>Parkinson disease</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term>
<term>Pathologie du système nerveux</term>
<term>Inflammation</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 Ml). 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>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0>
</fA01>
<fA03 i2="1"><s0>Mov. disord.</s0>
</fA03>
<fA05><s2>23</s2>
</fA05>
<fA06><s2>7</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Antineuronal Antibodies in Parkinson's Disease</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>VAN DE WARRENBURG (Bart P. C.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>CHURCH (Andrew J.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>MARTINO (Davide)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>CANDLER (Paul M.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>BHATIA (Kailash P.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>GIOVANNONI (Gavin)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>QUINN (Niall P.)</s1>
</fA11>
<fA14 i1="01"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Neurology, Radboud University Nijmegen Medical Centre</s1>
<s2>Nijmegen</s2>
<s3>NLD</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Neuroimmunology, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Neurological and Psychiatric Sciences, University of Bari</s1>
<s2>Bari</s2>
<s3>ITA</s3>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Institute of Cell and Molecular Science, Queen Mary University London and the Department of Neurology, Barts and The London NHS Trust</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA20><s1>958-963</s1>
</fA20>
<fA21><s1>2008</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000200276040050</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2008 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>22 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>08-0305144</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Movement disorders</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>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 Ml). 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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Inflammation</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Inflammation</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Inflamación</s0>
<s5>09</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>40</s5>
</fC07>
<fN21><s1>189</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 08-0305144 INIST</NO>
<ET>Antineuronal Antibodies in Parkinson's Disease</ET>
<AU>VAN DE WARRENBURG (Bart P. C.); CHURCH (Andrew J.); MARTINO (Davide); CANDLER (Paul M.); BHATIA (Kailash P.); GIOVANNONI (Gavin); QUINN (Niall P.)</AU>
<AF>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology/London/Royaume-Uni (1 aut., 3 aut., 5 aut., 7 aut.); Department of Neurology, Radboud University Nijmegen Medical Centre/Nijmegen/Pays-Bas (1 aut.); Department of Neuroimmunology, Institute of Neurology/London/Royaume-Uni (2 aut., 3 aut., 4 aut.); Department of Neurological and Psychiatric Sciences, University of Bari/Bari/Italie (3 aut.); Institute of Cell and Molecular Science, Queen Mary University London and the Department of Neurology, Barts and The London NHS Trust/London/Royaume-Uni (6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2008; Vol. 23; No. 7; Pp. 958-963; Bibl. 22 ref.</SO>
<LA>Anglais</LA>
<EA>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 Ml). 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.</EA>
<CC>002B17; 002B17G</CC>
<FD>Maladie de Parkinson; Pathologie du système nerveux; Inflammation</FD>
<FG>Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central</FG>
<ED>Parkinson disease; Nervous system diseases; Inflammation</ED>
<EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG>
<SD>Parkinson enfermedad; Sistema nervioso patología; Inflamación</SD>
<LO>INIST-20953.354000200276040050</LO>
<ID>08-0305144</ID>
</server>
</inist>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/PascalFrancis/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001238 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 001238 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Santé |area= MovDisordV3 |flux= PascalFrancis |étape= Corpus |type= RBID |clé= Pascal:08-0305144 |texte= Antineuronal Antibodies in Parkinson's Disease }}
This area was generated with Dilib version V0.6.23. |