Neuropathological spectrum of Synucleinopathies
Identifieur interne :
000934 ( PascalFrancis/Curation );
précédent :
000933;
suivant :
000935
Neuropathological spectrum of Synucleinopathies
Auteurs : Kurt A. Jellinger [
Autriche]
Source :
-
Movement disorders [ 0885-3185 ] ; 2003.
RBID : Pascal:04-0080428
Descripteurs français
English descriptors
Abstract
Synucleinopathies comprise a diverse group of neurodegenerative proteinopathies that share common pathological lesions composed of aggregates of conformational and posttranslational modifications of α-synuclein in selected populations of neurons and glia. Abnormal filamentous aggregates of misfolded α-synuclein protein are the major components of Lewy bodies, dystrophic (Lewy) neurites, and the Papp-Lantos filaments in oligodendroglia and neurons in multiple system atrophy linked to degeneration of affected brain regions. The synucleinopathies include (1) Lewy body disorders and dementia with Lewy bodies, (2) multiple system atrophy (MSA), and (3) Hallervorden-Spatz disease. (I) The pathological diagnosis of Lewy body disorders and dementia with Lewy bodies is established by validated consensus criteria based on semiquantitative assessment of subcortical and cortical Lewy bodies as their common hallmarks. They are accompanied by subcortical multisystem degeneration with neuronal loss and gliosis with or without Alzheimer pathologic state. Lewy bodies also occur in numerous other disorders, including pure autonomic failure, neuroaxonal dystrophies, and various amyloidoses and tauopathies. (2) Multiple system atrophy, a sporadic, adult-onset degenerative movement disorder of unknown cause, is characterized by α-synuclein-positive glial cytoplasmic and rare neuronal inclusions throughout the central nervous system associated with striatonigral degeneration, olivopontocerebellar atrophy, and involvement of medullar and spinal autonomic nuclei. (3) In neurodegeneration with brain iron accumulation type I, or Hallervorden-Spatz disease, α-synuclein is present in axonal spheroids and glial and neuronal inclusions. While the identity of the major components of Lewy bodies suggests that a pathway leading from normal soluble to abnormal misfolded filamentous proteins is central for their pathogenesis, regardless of the primary disorder, there are conformational differences in α-synuclein between neuronal and glial aggregates, showing nonuniform mapping for its epitopes. Despite several cellular and transgenic models, it is not clear whether inclusion body formation is an adaptive/ neuroprotective or a pathogenic reaction/process generated in response to different, mostly undetermined, functional triggers linked to neurodegeneration.
pA |
A01 | 01 | 1 | | @0 0885-3185 |
---|
A03 | | 1 | | @0 Mov. disord. |
---|
A05 | | | | @2 18 |
---|
A06 | | | | @2 6 @3 SUP |
---|
A08 | 01 | 1 | ENG | @1 Neuropathological spectrum of Synucleinopathies |
---|
A09 | 01 | 1 | ENG | @1 Parkinsonism and Dementia: Synucleinopathies, Tauopathies, and Beyond. Proceedings of the "Movement" Disorder Society-European Division-Sponsored Workshop, Istanbul, Turkey, 9-11 May 2002 |
---|
A11 | 01 | 1 | | @1 JELLINGER (Kurt A.) |
---|
A14 | 01 | | | @1 Institute of Clinical Neurobiology @2 Vienna @3 AUT @Z 1 aut. |
---|
A18 | 01 | 1 | | @1 "Movement" Disorder Society. European Division @2 Milwaukee, Wisconsin @3 USA @9 patr. |
---|
A20 | | | | @2 S2-S3 |
---|
A21 | | | | @1 2003 |
---|
A23 | 01 | | | @0 ENG |
---|
A43 | 01 | | | @1 INIST @2 20953 @5 354000113058290010 |
---|
A44 | | | | @0 0000 @1 © 2004 INIST-CNRS. All rights reserved. |
---|
A45 | | | | @0 77 ref. |
---|
A47 | 01 | 1 | | @0 04-0080428 |
---|
A60 | | | | @1 P @2 C |
---|
A61 | | | | @0 A |
---|
A64 | 01 | 1 | | @0 Movement disorders |
---|
A66 | 01 | | | @0 USA |
---|
C01 | 01 | | ENG | @0 Synucleinopathies comprise a diverse group of neurodegenerative proteinopathies that share common pathological lesions composed of aggregates of conformational and posttranslational modifications of α-synuclein in selected populations of neurons and glia. Abnormal filamentous aggregates of misfolded α-synuclein protein are the major components of Lewy bodies, dystrophic (Lewy) neurites, and the Papp-Lantos filaments in oligodendroglia and neurons in multiple system atrophy linked to degeneration of affected brain regions. The synucleinopathies include (1) Lewy body disorders and dementia with Lewy bodies, (2) multiple system atrophy (MSA), and (3) Hallervorden-Spatz disease. (I) The pathological diagnosis of Lewy body disorders and dementia with Lewy bodies is established by validated consensus criteria based on semiquantitative assessment of subcortical and cortical Lewy bodies as their common hallmarks. They are accompanied by subcortical multisystem degeneration with neuronal loss and gliosis with or without Alzheimer pathologic state. Lewy bodies also occur in numerous other disorders, including pure autonomic failure, neuroaxonal dystrophies, and various amyloidoses and tauopathies. (2) Multiple system atrophy, a sporadic, adult-onset degenerative movement disorder of unknown cause, is characterized by α-synuclein-positive glial cytoplasmic and rare neuronal inclusions throughout the central nervous system associated with striatonigral degeneration, olivopontocerebellar atrophy, and involvement of medullar and spinal autonomic nuclei. (3) In neurodegeneration with brain iron accumulation type I, or Hallervorden-Spatz disease, α-synuclein is present in axonal spheroids and glial and neuronal inclusions. While the identity of the major components of Lewy bodies suggests that a pathway leading from normal soluble to abnormal misfolded filamentous proteins is central for their pathogenesis, regardless of the primary disorder, there are conformational differences in α-synuclein between neuronal and glial aggregates, showing nonuniform mapping for its epitopes. Despite several cellular and transgenic models, it is not clear whether inclusion body formation is an adaptive/ neuroprotective or a pathogenic reaction/process generated in response to different, mostly undetermined, functional triggers linked to neurodegeneration. |
---|
C02 | 01 | X | | @0 002B17G |
---|
C03 | 01 | X | FRE | @0 Démence corps Lewy @2 NM @5 01 |
---|
C03 | 01 | X | ENG | @0 Lewy body dementia @2 NM @5 01 |
---|
C03 | 01 | X | SPA | @0 Demencia cuerpos Lewy @2 NM @5 01 |
---|
C03 | 02 | X | FRE | @0 Atrophie multisystématisée @2 NM @5 04 |
---|
C03 | 02 | X | ENG | @0 Multiple system atrophy @2 NM @5 04 |
---|
C03 | 02 | X | SPA | @0 Atrofia multisistematizada @2 NM @5 04 |
---|
C03 | 03 | X | FRE | @0 Corps inclusion @5 07 |
---|
C03 | 03 | X | ENG | @0 Inclusion body @5 07 |
---|
C03 | 03 | X | SPA | @0 Cuerpo inclusión @5 07 |
---|
C03 | 04 | X | FRE | @0 Anatomopathologie @5 10 |
---|
C03 | 04 | X | ENG | @0 Anatomic pathology @5 10 |
---|
C03 | 04 | X | SPA | @0 Anatomía patológica @5 10 |
---|
C03 | 05 | X | FRE | @0 Symptomatologie @5 17 |
---|
C03 | 05 | X | ENG | @0 Symptomatology @5 17 |
---|
C03 | 05 | X | SPA | @0 Sintomatología @5 17 |
---|
C03 | 06 | X | FRE | @0 Exploration @5 18 |
---|
C03 | 06 | X | ENG | @0 Exploration @5 18 |
---|
C03 | 06 | X | SPA | @0 Exploración @5 18 |
---|
C03 | 07 | X | FRE | @0 Homme @5 20 |
---|
C03 | 07 | X | ENG | @0 Human @5 20 |
---|
C03 | 07 | X | SPA | @0 Hombre @5 20 |
---|
C03 | 08 | X | FRE | @0 α-Synucléine @4 CD @5 96 |
---|
C03 | 08 | X | ENG | @0 Synuclein @4 CD @5 96 |
---|
C07 | 01 | X | FRE | @0 Système nerveux pathologie @5 37 |
---|
C07 | 01 | X | ENG | @0 Nervous system diseases @5 37 |
---|
C07 | 01 | X | SPA | @0 Sistema nervioso patología @5 37 |
---|
C07 | 02 | X | FRE | @0 Système nerveux central pathologie @5 38 |
---|
C07 | 02 | X | ENG | @0 Central nervous system disease @5 38 |
---|
C07 | 02 | X | SPA | @0 Sistema nervosio central patología @5 38 |
---|
C07 | 03 | X | FRE | @0 Encéphale pathologie @5 39 |
---|
C07 | 03 | X | ENG | @0 Cerebral disorder @5 39 |
---|
C07 | 03 | X | SPA | @0 Encéfalo patología @5 39 |
---|
C07 | 04 | X | FRE | @0 Maladie dégénérative @5 40 |
---|
C07 | 04 | X | ENG | @0 Degenerative disease @5 40 |
---|
C07 | 04 | X | SPA | @0 Enfermedad degenerativa @5 40 |
---|
N21 | | | | @1 054 |
---|
N82 | | | | @1 PSI |
---|
|
pR |
A30 | 01 | 1 | ENG | @1 Parkinsonism and Dementia: Sinucleinopathies, Tauopathies, and Beyond. Workshop @3 Istanbul TUR @4 2002-05-09 |
---|
|
Links toward previous steps (curation, corpus...)
- to stream PascalFrancis, to step Corpus: Pour aller vers cette notice dans l'étape Curation :002387
Links to Exploration step
Pascal:04-0080428
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Neuropathological spectrum of Synucleinopathies</title>
<author><name sortKey="Jellinger, Kurt A" sort="Jellinger, Kurt A" uniqKey="Jellinger K" first="Kurt A." last="Jellinger">Kurt A. Jellinger</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Institute of Clinical Neurobiology</s1>
<s2>Vienna</s2>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
<country>Autriche</country>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">04-0080428</idno>
<date when="2003">2003</date>
<idno type="stanalyst">PASCAL 04-0080428 INIST</idno>
<idno type="RBID">Pascal:04-0080428</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">002387</idno>
<idno type="wicri:Area/PascalFrancis/Curation">000934</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Neuropathological spectrum of Synucleinopathies</title>
<author><name sortKey="Jellinger, Kurt A" sort="Jellinger, Kurt A" uniqKey="Jellinger K" first="Kurt A." last="Jellinger">Kurt A. Jellinger</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Institute of Clinical Neurobiology</s1>
<s2>Vienna</s2>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
<country>Autriche</country>
</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="2003">2003</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>Anatomic pathology</term>
<term>Exploration</term>
<term>Human</term>
<term>Inclusion body</term>
<term>Lewy body dementia</term>
<term>Multiple system atrophy</term>
<term>Symptomatology</term>
<term>Synuclein</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Démence corps Lewy</term>
<term>Atrophie multisystématisée</term>
<term>Corps inclusion</term>
<term>Anatomopathologie</term>
<term>Symptomatologie</term>
<term>Exploration</term>
<term>Homme</term>
<term>α-Synucléine</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Synucleinopathies comprise a diverse group of neurodegenerative proteinopathies that share common pathological lesions composed of aggregates of conformational and posttranslational modifications of α-synuclein in selected populations of neurons and glia. Abnormal filamentous aggregates of misfolded α-synuclein protein are the major components of Lewy bodies, dystrophic (Lewy) neurites, and the Papp-Lantos filaments in oligodendroglia and neurons in multiple system atrophy linked to degeneration of affected brain regions. The synucleinopathies include (1) Lewy body disorders and dementia with Lewy bodies, (2) multiple system atrophy (MSA), and (3) Hallervorden-Spatz disease. (I) The pathological diagnosis of Lewy body disorders and dementia with Lewy bodies is established by validated consensus criteria based on semiquantitative assessment of subcortical and cortical Lewy bodies as their common hallmarks. They are accompanied by subcortical multisystem degeneration with neuronal loss and gliosis with or without Alzheimer pathologic state. Lewy bodies also occur in numerous other disorders, including pure autonomic failure, neuroaxonal dystrophies, and various amyloidoses and tauopathies. (2) Multiple system atrophy, a sporadic, adult-onset degenerative movement disorder of unknown cause, is characterized by α-synuclein-positive glial cytoplasmic and rare neuronal inclusions throughout the central nervous system associated with striatonigral degeneration, olivopontocerebellar atrophy, and involvement of medullar and spinal autonomic nuclei. (3) In neurodegeneration with brain iron accumulation type I, or Hallervorden-Spatz disease, α-synuclein is present in axonal spheroids and glial and neuronal inclusions. While the identity of the major components of Lewy bodies suggests that a pathway leading from normal soluble to abnormal misfolded filamentous proteins is central for their pathogenesis, regardless of the primary disorder, there are conformational differences in α-synuclein between neuronal and glial aggregates, showing nonuniform mapping for its epitopes. Despite several cellular and transgenic models, it is not clear whether inclusion body formation is an adaptive/ neuroprotective or a pathogenic reaction/process generated in response to different, mostly undetermined, functional triggers linked to neurodegeneration.</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>
<fA06><s2>6</s2>
<s3>SUP</s3>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Neuropathological spectrum of Synucleinopathies</s1>
</fA08>
<fA09 i1="01" i2="1" l="ENG"><s1>Parkinsonism and Dementia: Synucleinopathies, Tauopathies, and Beyond. Proceedings of the "Movement" Disorder Society-European Division-Sponsored Workshop, Istanbul, Turkey, 9-11 May 2002</s1>
</fA09>
<fA11 i1="01" i2="1"><s1>JELLINGER (Kurt A.)</s1>
</fA11>
<fA14 i1="01"><s1>Institute of Clinical Neurobiology</s1>
<s2>Vienna</s2>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA18 i1="01" i2="1"><s1>"Movement" Disorder Society. European Division</s1>
<s2>Milwaukee, Wisconsin</s2>
<s3>USA</s3>
<s9>patr.</s9>
</fA18>
<fA20><s2>S2-S3</s2>
</fA20>
<fA21><s1>2003</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000113058290010</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2004 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>77 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>04-0080428</s0>
</fA47>
<fA60><s1>P</s1>
<s2>C</s2>
</fA60>
<fA64 i1="01" i2="1"><s0>Movement disorders</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Synucleinopathies comprise a diverse group of neurodegenerative proteinopathies that share common pathological lesions composed of aggregates of conformational and posttranslational modifications of α-synuclein in selected populations of neurons and glia. Abnormal filamentous aggregates of misfolded α-synuclein protein are the major components of Lewy bodies, dystrophic (Lewy) neurites, and the Papp-Lantos filaments in oligodendroglia and neurons in multiple system atrophy linked to degeneration of affected brain regions. The synucleinopathies include (1) Lewy body disorders and dementia with Lewy bodies, (2) multiple system atrophy (MSA), and (3) Hallervorden-Spatz disease. (I) The pathological diagnosis of Lewy body disorders and dementia with Lewy bodies is established by validated consensus criteria based on semiquantitative assessment of subcortical and cortical Lewy bodies as their common hallmarks. They are accompanied by subcortical multisystem degeneration with neuronal loss and gliosis with or without Alzheimer pathologic state. Lewy bodies also occur in numerous other disorders, including pure autonomic failure, neuroaxonal dystrophies, and various amyloidoses and tauopathies. (2) Multiple system atrophy, a sporadic, adult-onset degenerative movement disorder of unknown cause, is characterized by α-synuclein-positive glial cytoplasmic and rare neuronal inclusions throughout the central nervous system associated with striatonigral degeneration, olivopontocerebellar atrophy, and involvement of medullar and spinal autonomic nuclei. (3) In neurodegeneration with brain iron accumulation type I, or Hallervorden-Spatz disease, α-synuclein is present in axonal spheroids and glial and neuronal inclusions. While the identity of the major components of Lewy bodies suggests that a pathway leading from normal soluble to abnormal misfolded filamentous proteins is central for their pathogenesis, regardless of the primary disorder, there are conformational differences in α-synuclein between neuronal and glial aggregates, showing nonuniform mapping for its epitopes. Despite several cellular and transgenic models, it is not clear whether inclusion body formation is an adaptive/ neuroprotective or a pathogenic reaction/process generated in response to different, mostly undetermined, functional triggers linked to neurodegeneration.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Démence corps Lewy</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Lewy body dementia</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Demencia cuerpos Lewy</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Atrophie multisystématisée</s0>
<s2>NM</s2>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Multiple system atrophy</s0>
<s2>NM</s2>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Atrofia multisistematizada</s0>
<s2>NM</s2>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Corps inclusion</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Inclusion body</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Cuerpo inclusión</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Anatomopathologie</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Anatomic pathology</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Anatomía patológica</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Symptomatologie</s0>
<s5>17</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Symptomatology</s0>
<s5>17</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Sintomatología</s0>
<s5>17</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Exploration</s0>
<s5>18</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Exploration</s0>
<s5>18</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Exploración</s0>
<s5>18</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>α-Synucléine</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Synuclein</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>40</s5>
</fC07>
<fN21><s1>054</s1>
</fN21>
<fN82><s1>PSI</s1>
</fN82>
</pA>
<pR><fA30 i1="01" i2="1" l="ENG"><s1>Parkinsonism and Dementia: Sinucleinopathies, Tauopathies, and Beyond. Workshop</s1>
<s3>Istanbul TUR</s3>
<s4>2002-05-09</s4>
</fA30>
</pR>
</standard>
</inist>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/PascalFrancis/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000934 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Curation/biblio.hfd -nk 000934 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= PascalFrancis
|étape= Curation
|type= RBID
|clé= Pascal:04-0080428
|texte= Neuropathological spectrum of Synucleinopathies
}}
| This area was generated with Dilib version V0.6.23. Data generation: Sun Jul 3 12:29:32 2016. Site generation: Wed Feb 14 10:52:30 2024 | ![](Common/icons/LogoDilib.gif) |