Atypical parkinsonism combining alpha-synuclein inclusions and polyglucosan body disease.
Identifieur interne : 000F57 ( Ncbi/Checkpoint ); précédent : 000F56; suivant : 000F58Atypical parkinsonism combining alpha-synuclein inclusions and polyglucosan body disease.
Auteurs : Elsa Krim [France] ; Anne Vital ; Frederic Macia ; Farid Yekhlef ; François TisonSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2005.
English descriptors
- KwdEn :
- Aged, Glial Fibrillary Acidic Protein (metabolism), Glucans (metabolism), Humans, Immunohistochemistry (methods), Inclusion Bodies (metabolism), Inclusion Bodies (pathology), Lewy Bodies (metabolism), Lewy Bodies (pathology), Male, Multiple System Atrophy (etiology), Multiple System Atrophy (pathology), Nerve Tissue Proteins (metabolism), Parkinsonian Disorders (complications), Parkinsonian Disorders (metabolism), Parkinsonian Disorders (pathology), Review Literature as Topic, Staining and Labeling (methods), Synucleins, alpha-Synuclein.
- MESH :
- chemical , metabolism : Glial Fibrillary Acidic Protein, Glucans, Nerve Tissue Proteins.
- complications : Parkinsonian Disorders.
- etiology : Multiple System Atrophy.
- metabolism : Inclusion Bodies, Lewy Bodies, Parkinsonian Disorders.
- methods : Immunohistochemistry, Staining and Labeling.
- pathology : Inclusion Bodies, Lewy Bodies, Multiple System Atrophy, Parkinsonian Disorders.
- Aged, Humans, Male, Review Literature as Topic, Synucleins, alpha-Synuclein.
Abstract
Adult polyglucosan body disease (APGBD) is a rare disorder affecting the central and peripheral nervous systems and in which parkinsonism is unusual. A 71-year-old man presented levodopa-unresponsive parkinsonism with urinary incontinence and recurrent syncopes of 6 years standing masquerading as atypical parkinsonism of the multiple system atrophy (MSA-P) type. Brain histopathology demonstrated massive accumulation of polyglucosan bodies particularly in the putamen. In addition, there were dense alpha-synuclein-positive cytoplasmic oligodendroglial inclusions in the pons and in the middle cerebellar peduncle. These inclusions may be either due to the chance association of MSA-P with APGBD, or pathologically related to APGBD.
DOI: 10.1002/mds.20285
PubMed: 15382212
Affiliations:
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pubmed:15382212Le document en format XML
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Macia</name></author><author><name sortKey="Yekhlef, Farid" sort="Yekhlef, Farid" uniqKey="Yekhlef F" first="Farid" last="Yekhlef">Farid Yekhlef</name></author><author><name sortKey="Tison, Francois" sort="Tison, Francois" uniqKey="Tison F" first="François" last="Tison">François Tison</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:15382212</idno><idno type="pmid">15382212</idno><idno type="doi">10.1002/mds.20285</idno><idno type="wicri:Area/PubMed/Corpus">003331</idno><idno type="wicri:Area/PubMed/Curation">003331</idno><idno type="wicri:Area/PubMed/Checkpoint">003224</idno><idno type="wicri:Area/Ncbi/Merge">000F57</idno><idno type="wicri:Area/Ncbi/Curation">000F57</idno><idno type="wicri:Area/Ncbi/Checkpoint">000F57</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Atypical parkinsonism combining alpha-synuclein inclusions and polyglucosan body 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Yekhlef</name></author><author><name sortKey="Tison, Francois" sort="Tison, Francois" uniqKey="Tison F" first="François" last="Tison">François Tison</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Glial Fibrillary Acidic Protein (metabolism)</term><term>Glucans (metabolism)</term><term>Humans</term><term>Immunohistochemistry (methods)</term><term>Inclusion Bodies (metabolism)</term><term>Inclusion Bodies (pathology)</term><term>Lewy Bodies (metabolism)</term><term>Lewy Bodies (pathology)</term><term>Male</term><term>Multiple System Atrophy (etiology)</term><term>Multiple System Atrophy (pathology)</term><term>Nerve Tissue Proteins (metabolism)</term><term>Parkinsonian Disorders (complications)</term><term>Parkinsonian Disorders (metabolism)</term><term>Parkinsonian Disorders (pathology)</term><term>Review Literature as Topic</term><term>Staining and Labeling (methods)</term><term>Synucleins</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glial Fibrillary Acidic Protein</term><term>Glucans</term><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Multiple System Atrophy</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Inclusion Bodies</term><term>Lewy Bodies</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Immunohistochemistry</term><term>Staining and Labeling</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inclusion Bodies</term><term>Lewy Bodies</term><term>Multiple System Atrophy</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Humans</term><term>Male</term><term>Review Literature as Topic</term><term>Synucleins</term><term>alpha-Synuclein</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Adult polyglucosan body disease (APGBD) is a rare disorder affecting the central and peripheral nervous systems and in which parkinsonism is unusual. A 71-year-old man presented levodopa-unresponsive parkinsonism with urinary incontinence and recurrent syncopes of 6 years standing masquerading as atypical parkinsonism of the multiple system atrophy (MSA-P) type. Brain histopathology demonstrated massive accumulation of polyglucosan bodies particularly in the putamen. In addition, there were dense alpha-synuclein-positive cytoplasmic oligodendroglial inclusions in the pons and in the middle cerebellar peduncle. These inclusions may be either due to the chance association of MSA-P with APGBD, or pathologically related to APGBD.</div></front></TEI><affiliations><list><country><li>France</li></country></list><tree><noCountry><name sortKey="Macia, Frederic" sort="Macia, Frederic" uniqKey="Macia F" first="Frederic" last="Macia">Frederic Macia</name><name sortKey="Tison, Francois" sort="Tison, Francois" uniqKey="Tison F" first="François" last="Tison">François Tison</name><name sortKey="Vital, Anne" sort="Vital, Anne" uniqKey="Vital A" first="Anne" last="Vital">Anne Vital</name><name sortKey="Yekhlef, Farid" sort="Yekhlef, Farid" uniqKey="Yekhlef F" first="Farid" last="Yekhlef">Farid Yekhlef</name></noCountry><country name="France"><noRegion><name sortKey="Krim, Elsa" sort="Krim, Elsa" uniqKey="Krim E" first="Elsa" last="Krim">Elsa Krim</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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