Corticobasal syndrome with novel argyrophilic glial inclusions
Identifieur interne : 005053 ( Main/Merge ); précédent : 005052; suivant : 005054Corticobasal syndrome with novel argyrophilic glial inclusions
Auteurs : Gregory A. Rippon [États-Unis] ; S. M. Staugaitis [États-Unis] ; Steven S. M. Chin [États-Unis] ; James E. Goldman [États-Unis] ; K. Marder [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2005-05.
English descriptors
- KwdEn :
- Adult, Apraxia, Ideomotor (complications), Apraxia, Ideomotor (metabolism), Apraxia, Ideomotor (pathology), Atrophy (pathology), Basal Ganglia (metabolism), Basal Ganglia (pathology), Dysarthria (complications), Fatal Outcome, Female, Frontal Lobe (pathology), Glial Fibrillary Acidic Protein (metabolism), Humans, Muscle Rigidity (complications), Muscle Rigidity (metabolism), Muscle Rigidity (pathology), Nerve Degeneration (complications), Nerve Degeneration (metabolism), Nerve Degeneration (pathology), Syndrome, Ubiquitin (immunology), Ubiquitin (metabolism), alpha-Crystallins (immunology), alpha-Crystallins (metabolism), corticobasal degeneration, corticobasal syndrome, degenerative disorders, glial inclusions, neuropathology.
- MESH :
- chemical , immunology : Ubiquitin, alpha-Crystallins.
- chemical , metabolism : Glial Fibrillary Acidic Protein, Ubiquitin, alpha-Crystallins.
- complications : Apraxia, Ideomotor, Dysarthria, Muscle Rigidity, Nerve Degeneration.
- metabolism : Apraxia, Ideomotor, Basal Ganglia, Muscle Rigidity, Nerve Degeneration.
- pathology : Apraxia, Ideomotor, Atrophy, Basal Ganglia, Frontal Lobe, Muscle Rigidity, Nerve Degeneration.
- Adult, Fatal Outcome, Female, Humans, Syndrome.
Abstract
A 42‐year‐old, left‐handed woman first noted impaired dexterity of the dominant hand, soon followed by dysarthria and cognitive decline. Over a 4‐year period, she developed severe left‐sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single‐photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and αB‐crystallin but not to microtubule‐associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or α‐synuclein. The argyrophilic inclusions identified in this case are distinct from those previously described in neurodegenerative diseases. © 2005 Movement Disorder Society
Url:
DOI: 10.1002/mds.20396
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-05">2005-05</date><biblScope unit="vol">20</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="598">598</biblScope><biblScope unit="page" to="602">602</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">32F8EA69F6D8D6CDA861CBF1801566B9FA9D60E6</idno><idno type="DOI">10.1002/mds.20396</idno><idno type="ArticleID">MDS20396</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Apraxia, Ideomotor (complications)</term><term>Apraxia, Ideomotor (metabolism)</term><term>Apraxia, Ideomotor (pathology)</term><term>Atrophy (pathology)</term><term>Basal Ganglia (metabolism)</term><term>Basal Ganglia (pathology)</term><term>Dysarthria (complications)</term><term>Fatal Outcome</term><term>Female</term><term>Frontal Lobe (pathology)</term><term>Glial Fibrillary Acidic Protein (metabolism)</term><term>Humans</term><term>Muscle Rigidity (complications)</term><term>Muscle Rigidity (metabolism)</term><term>Muscle Rigidity (pathology)</term><term>Nerve Degeneration (complications)</term><term>Nerve Degeneration (metabolism)</term><term>Nerve Degeneration (pathology)</term><term>Syndrome</term><term>Ubiquitin (immunology)</term><term>Ubiquitin (metabolism)</term><term>alpha-Crystallins (immunology)</term><term>alpha-Crystallins (metabolism)</term><term>corticobasal degeneration</term><term>corticobasal syndrome</term><term>degenerative disorders</term><term>glial inclusions</term><term>neuropathology</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Ubiquitin</term><term>alpha-Crystallins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glial Fibrillary Acidic Protein</term><term>Ubiquitin</term><term>alpha-Crystallins</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Apraxia, Ideomotor</term><term>Dysarthria</term><term>Muscle Rigidity</term><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Apraxia, Ideomotor</term><term>Basal Ganglia</term><term>Muscle Rigidity</term><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Apraxia, Ideomotor</term><term>Atrophy</term><term>Basal Ganglia</term><term>Frontal Lobe</term><term>Muscle Rigidity</term><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Fatal Outcome</term><term>Female</term><term>Humans</term><term>Syndrome</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A 42‐year‐old, left‐handed woman first noted impaired dexterity of the dominant hand, soon followed by dysarthria and cognitive decline. Over a 4‐year period, she developed severe left‐sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single‐photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and αB‐crystallin but not to microtubule‐associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or α‐synuclein. The argyrophilic inclusions identified in this case are distinct from those previously described in neurodegenerative diseases. © 2005 Movement Disorder Society</div></front></TEI><double doi="10.1002/mds.20396"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Corticobasal syndrome with novel argyrophilic glial inclusions</title><author><name sortKey="Rippon, Gregory A" sort="Rippon, Gregory A" uniqKey="Rippon G" first="Gregory A." last="Rippon">Gregory A. Rippon</name></author><author><name sortKey="Staugaitis, S M" sort="Staugaitis, S M" uniqKey="Staugaitis S" first="S. M." last="Staugaitis">S. M. Staugaitis</name></author><author><name sortKey="Chin, Steven S M" sort="Chin, Steven S M" uniqKey="Chin S" first="Steven S. M." last="Chin">Steven S. M. Chin</name></author><author><name sortKey="Goldman, James E" sort="Goldman, James E" uniqKey="Goldman J" first="James E." last="Goldman">James E. Goldman</name></author><author><name sortKey="Marder, K" sort="Marder, K" uniqKey="Marder K" first="K." last="Marder">K. Marder</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:32F8EA69F6D8D6CDA861CBF1801566B9FA9D60E6</idno><date when="2005" year="2005">2005</date><idno type="doi">10.1002/mds.20396</idno><idno type="url">https://api.istex.fr/document/32F8EA69F6D8D6CDA861CBF1801566B9FA9D60E6/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001D68</idno><idno type="wicri:Area/Istex/Curation">001D68</idno><idno type="wicri:Area/Istex/Checkpoint">002376</idno><idno type="wicri:doubleKey">0885-3185:2005:Rippon G:corticobasal:syndrome:with</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Corticobasal syndrome with novel argyrophilic glial inclusions</title><author><name sortKey="Rippon, Gregory A" sort="Rippon, Gregory A" uniqKey="Rippon G" first="Gregory A." last="Rippon">Gregory A. Rippon</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Gertrude H. Sergievsky Center, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region><settlement type="city">New York</settlement></placeName><orgName type="university">Université Columbia</orgName></affiliation><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region><settlement type="city">New York</settlement></placeName><orgName type="university">Université Columbia</orgName></affiliation></author><author><name sortKey="Staugaitis, S M" sort="Staugaitis, S M" uniqKey="Staugaitis S" first="S. M." last="Staugaitis">S. M. Staugaitis</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurosciences, Cleveland Clinic Foundation, Cleveland, Ohio</wicri:regionArea><placeName><region type="state">Ohio</region></placeName></affiliation></author><author><name sortKey="Chin, Steven S M" sort="Chin, Steven S M" uniqKey="Chin S" first="Steven S. M." last="Chin">Steven S. M. Chin</name><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region><settlement type="city">New York</settlement></placeName><orgName type="university">Université Columbia</orgName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Goldman, James E" sort="Goldman, James E" uniqKey="Goldman J" first="James E." last="Goldman">James E. Goldman</name><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region><settlement type="city">New York</settlement></placeName><orgName type="university">Université Columbia</orgName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Marder, K" sort="Marder, K" uniqKey="Marder K" first="K." last="Marder">K. Marder</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Gertrude H. Sergievsky Center, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region><settlement type="city">New York</settlement></placeName><orgName type="university">Université Columbia</orgName></affiliation><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region><settlement type="city">New York</settlement></placeName><orgName type="university">Université Columbia</orgName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Psychiatry, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-05">2005-05</date><biblScope unit="vol">20</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="598">598</biblScope><biblScope unit="page" to="602">602</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">32F8EA69F6D8D6CDA861CBF1801566B9FA9D60E6</idno><idno type="DOI">10.1002/mds.20396</idno><idno type="ArticleID">MDS20396</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>corticobasal degeneration</term><term>corticobasal syndrome</term><term>degenerative disorders</term><term>glial inclusions</term><term>neuropathology</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A 42‐year‐old, left‐handed woman first noted impaired dexterity of the dominant hand, soon followed by dysarthria and cognitive decline. Over a 4‐year period, she developed severe left‐sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single‐photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and αB‐crystallin but not to microtubule‐associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or α‐synuclein. The argyrophilic inclusions identified in this case are distinct from those previously described in neurodegenerative diseases. © 2005 Movement Disorder Society</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Corticobasal syndrome with novel argyrophilic glial inclusions.</title><author><name sortKey="Rippon, Gregory A" sort="Rippon, Gregory A" uniqKey="Rippon G" first="Gregory A" last="Rippon">Gregory A. Rippon</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA. grippon@sergievsky.cpmc.columbia.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York 10032</wicri:regionArea><wicri:noRegion>New York 10032</wicri:noRegion></affiliation></author><author><name sortKey="Staugaitis, S M" sort="Staugaitis, S M" uniqKey="Staugaitis S" first="S M" last="Staugaitis">S M Staugaitis</name></author><author><name sortKey="Chin, Steven S M" sort="Chin, Steven S M" uniqKey="Chin S" first="Steven S M" last="Chin">Steven S M. Chin</name></author><author><name sortKey="Goldman, James E" sort="Goldman, James E" uniqKey="Goldman J" first="James E" last="Goldman">James E. Goldman</name></author><author><name sortKey="Marder, K" sort="Marder, K" uniqKey="Marder K" first="K" last="Marder">K. Marder</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="doi">10.1002/mds.20396</idno><idno type="RBID">pubmed:15726537</idno><idno type="pmid">15726537</idno><idno type="wicri:Area/PubMed/Corpus">003139</idno><idno type="wicri:Area/PubMed/Curation">003139</idno><idno type="wicri:Area/PubMed/Checkpoint">003178</idno><idno type="wicri:Area/Ncbi/Merge">001162</idno><idno type="wicri:Area/Ncbi/Curation">001162</idno><idno type="wicri:Area/Ncbi/Checkpoint">001162</idno><idno type="wicri:doubleKey">0885-3185:2005:Rippon G:corticobasal:syndrome:with</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Corticobasal syndrome with novel argyrophilic glial inclusions.</title><author><name sortKey="Rippon, Gregory A" sort="Rippon, Gregory A" uniqKey="Rippon G" first="Gregory A" last="Rippon">Gregory A. Rippon</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA. grippon@sergievsky.cpmc.columbia.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York 10032</wicri:regionArea><wicri:noRegion>New York 10032</wicri:noRegion></affiliation></author><author><name sortKey="Staugaitis, S M" sort="Staugaitis, S M" uniqKey="Staugaitis S" first="S M" last="Staugaitis">S M Staugaitis</name></author><author><name sortKey="Chin, Steven S M" sort="Chin, Steven S M" uniqKey="Chin S" first="Steven S M" last="Chin">Steven S M. Chin</name></author><author><name sortKey="Goldman, James E" sort="Goldman, James E" uniqKey="Goldman J" first="James E" last="Goldman">James E. Goldman</name></author><author><name sortKey="Marder, K" sort="Marder, K" uniqKey="Marder K" first="K" last="Marder">K. Marder</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>Adult</term><term>Apraxia, Ideomotor (complications)</term><term>Apraxia, Ideomotor (metabolism)</term><term>Apraxia, Ideomotor (pathology)</term><term>Atrophy (pathology)</term><term>Basal Ganglia (metabolism)</term><term>Basal Ganglia (pathology)</term><term>Dysarthria (complications)</term><term>Fatal Outcome</term><term>Female</term><term>Frontal Lobe (pathology)</term><term>Glial Fibrillary Acidic Protein (metabolism)</term><term>Humans</term><term>Muscle Rigidity (complications)</term><term>Muscle Rigidity (metabolism)</term><term>Muscle Rigidity (pathology)</term><term>Nerve Degeneration (complications)</term><term>Nerve Degeneration (metabolism)</term><term>Nerve Degeneration (pathology)</term><term>Syndrome</term><term>Ubiquitin (immunology)</term><term>Ubiquitin (metabolism)</term><term>alpha-Crystallins (immunology)</term><term>alpha-Crystallins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Ubiquitin</term><term>alpha-Crystallins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glial Fibrillary Acidic Protein</term><term>Ubiquitin</term><term>alpha-Crystallins</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Apraxia, Ideomotor</term><term>Dysarthria</term><term>Muscle Rigidity</term><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Apraxia, Ideomotor</term><term>Basal Ganglia</term><term>Muscle Rigidity</term><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Apraxia, Ideomotor</term><term>Atrophy</term><term>Basal Ganglia</term><term>Frontal Lobe</term><term>Muscle Rigidity</term><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Fatal Outcome</term><term>Female</term><term>Humans</term><term>Syndrome</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A 42-year-old, left-handed woman first noted impaired dexterity of the dominant hand, soon followed by dysarthria and cognitive decline. Over a 4-year period, she developed severe left-sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single-photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and alphaB-crystallin but not to microtubule-associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or alpha-synuclein. The argyrophilic inclusions identified in this case are distinct from those previously described in neurodegenerative diseases.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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