In vitro models of multiple system atrophy
Identifieur interne :
000F49 ( PascalFrancis/Curation );
précédent :
000F48;
suivant :
000F50
In vitro models of multiple system atrophy
Auteurs : Nadia Stefanova [
Autriche] ;
Markus Reindl [
Autriche] ;
Werner Poewe [
Autriche] ;
Gregor K. Wenning [
Autriche]
Source :
-
Movement disorders [ 0885-3185 ] ; 2005.
RBID : Pascal:05-0457543
Descripteurs français
English descriptors
Abstract
α-Synuclein represents the major constituent of oligodendroglial cytoplasmic inclusions, the hallmark lesion of multiple system atrophy (MSA), a progressive disorder that is associated with selective degenerative cell loss in basal ganglia, cerebellum, brainstem, and spinal cord. The role of abnormal α-synuclein aggregation in oligodendroglial cells is still obscure, in particular, whether α-synuclein might impair oligodendroglial and, secondarily, neuronal integrity of those cells in the diseased brain. In an attempt to answer some of these questions, we have developed an "in vitro model of MSA" by expressing the wild-type or C-terminally truncated form of α-synuclein in glial cell cultures. With this simplified system, we have demonstrated that α-synuclein significantly affects the survival of glia and its vulnerability to environmental stress, which might represent a major step in the pathogenesis of MSA.
| pA |
| A01 | 01 | 1 | | @0 0885-3185 |
|---|
| A03 | | 1 | | @0 Mov. disord. |
|---|
| A05 | | | | @2 20 |
|---|
| A06 | | | | @3 SUP12 |
|---|
| A08 | 01 | 1 | ENG | @1 In vitro models of multiple system atrophy |
|---|
| A09 | 01 | 1 | ENG | @1 Atypical Parkinsonian Disorders |
|---|
| A11 | 01 | 1 | | @1 STEFANOVA (Nadia) |
|---|
| A11 | 02 | 1 | | @1 REINDL (Markus) |
|---|
| A11 | 03 | 1 | | @1 POEWE (Werner) |
|---|
| A11 | 04 | 1 | | @1 WENNING (Gregor K.) |
|---|
| A12 | 01 | 1 | | @1 POEWE (Werner) @9 ed. |
|---|
| A12 | 02 | 1 | | @1 WENNING (Gregor K.) @9 ed. |
|---|
| A14 | 01 | | | @1 Neurological Research Laboratory, Department of Neurology, University Hospital of Innsbruck @3 AUT @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. |
|---|
| A15 | 01 | | | @1 Department of Neurology, Medical University Innsbruck @2 Innsbruck @3 AUT @Z 1 aut. @Z 2 aut. |
|---|
| A20 | | | | @2 S53-S56 |
|---|
| A21 | | | | @1 2005 |
|---|
| A23 | 01 | | | @0 ENG |
|---|
| A43 | 01 | | | @1 INIST @2 20953 @5 354000132714250080 |
|---|
| A44 | | | | @0 0000 @1 © 2005 INIST-CNRS. All rights reserved. |
|---|
| A45 | | | | @0 13 ref. |
|---|
| A47 | 01 | 1 | | @0 05-0457543 |
|---|
| A60 | | | | @1 P @2 C |
|---|
| A61 | | | | @0 A |
|---|
| A64 | 01 | 1 | | @0 Movement disorders |
|---|
| A66 | 01 | | | @0 USA |
|---|
| C01 | 01 | | ENG | @0 α-Synuclein represents the major constituent of oligodendroglial cytoplasmic inclusions, the hallmark lesion of multiple system atrophy (MSA), a progressive disorder that is associated with selective degenerative cell loss in basal ganglia, cerebellum, brainstem, and spinal cord. The role of abnormal α-synuclein aggregation in oligodendroglial cells is still obscure, in particular, whether α-synuclein might impair oligodendroglial and, secondarily, neuronal integrity of those cells in the diseased brain. In an attempt to answer some of these questions, we have developed an "in vitro model of MSA" by expressing the wild-type or C-terminally truncated form of α-synuclein in glial cell cultures. With this simplified system, we have demonstrated that α-synuclein significantly affects the survival of glia and its vulnerability to environmental stress, which might represent a major step in the pathogenesis of MSA. |
|---|
| C02 | 01 | X | | @0 002B17 |
|---|
| C02 | 02 | X | | @0 002B17F |
|---|
| C02 | 03 | X | | @0 002B17G |
|---|
| C03 | 01 | X | FRE | @0 Système nerveux pathologie @5 01 |
|---|
| C03 | 01 | X | ENG | @0 Nervous system diseases @5 01 |
|---|
| C03 | 01 | X | SPA | @0 Sistema nervioso patología @5 01 |
|---|
| C03 | 02 | X | FRE | @0 Atrophie multisystématisée @2 NM @5 02 |
|---|
| C03 | 02 | X | ENG | @0 Multiple system atrophy @2 NM @5 02 |
|---|
| C03 | 02 | X | SPA | @0 Atrofia multisistematizada @2 NM @5 02 |
|---|
| C03 | 03 | X | FRE | @0 Modèle @5 09 |
|---|
| C03 | 03 | X | ENG | @0 Models @5 09 |
|---|
| C03 | 03 | X | SPA | @0 Modelo @5 09 |
|---|
| C03 | 04 | X | FRE | @0 Inclusion @5 10 |
|---|
| C03 | 04 | X | ENG | @0 Inclusion @5 10 |
|---|
| C03 | 04 | X | SPA | @0 Inclusión @5 10 |
|---|
| N21 | | | | @1 318 |
|---|
| N44 | 01 | | | @1 OTO |
|---|
| N82 | | | | @1 OTO |
|---|
|
|---|
| pR |
| A30 | 01 | 1 | ENG | @1 Atypical Parkinsonian Disorders - From Protein Dysfunction to Therapeutic Intervention. International Meeting @3 Innsbruck AUT @4 2003-02-19 |
|---|
|
|---|
Links toward previous steps (curation, corpus...)
- to stream PascalFrancis, to step Corpus: Pour aller vers cette notice dans l'étape Curation :001D72
Links to Exploration step
Pascal:05-0457543
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">In vitro models of multiple system atrophy</title>
<author><name sortKey="Stefanova, Nadia" sort="Stefanova, Nadia" uniqKey="Stefanova N" first="Nadia" last="Stefanova">Nadia Stefanova</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurological Research Laboratory, Department of Neurology, University Hospital of Innsbruck</s1>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14><country>Autriche</country>
</affiliation><author><name sortKey="Reindl, Markus" sort="Reindl, Markus" uniqKey="Reindl M" first="Markus" last="Reindl">Markus Reindl</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurological Research Laboratory, Department of Neurology, University Hospital of Innsbruck</s1>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14><country>Autriche</country>
</affiliation><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurological Research Laboratory, Department of Neurology, University Hospital of Innsbruck</s1>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14><country>Autriche</country>
</affiliation><author><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K." last="Wenning">Gregor K. Wenning</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurological Research Laboratory, Department of Neurology, University Hospital of Innsbruck</s1>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14><country>Autriche</country>
</affiliation><publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">05-0457543</idno>
<date when="2005">2005</date>
<idno type="stanalyst">PASCAL 05-0457543 INIST</idno>
<idno type="RBID">Pascal:05-0457543</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">001D72</idno>
<idno type="wicri:Area/PascalFrancis/Curation">000F49</idno>
</publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">In vitro models of multiple system atrophy</title>
<author><name sortKey="Stefanova, Nadia" sort="Stefanova, Nadia" uniqKey="Stefanova N" first="Nadia" last="Stefanova">Nadia Stefanova</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurological Research Laboratory, Department of Neurology, University Hospital of Innsbruck</s1>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14><country>Autriche</country>
</affiliation><author><name sortKey="Reindl, Markus" sort="Reindl, Markus" uniqKey="Reindl M" first="Markus" last="Reindl">Markus Reindl</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurological Research Laboratory, Department of Neurology, University Hospital of Innsbruck</s1>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14><country>Autriche</country>
</affiliation><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurological Research Laboratory, Department of Neurology, University Hospital of Innsbruck</s1>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14><country>Autriche</country>
</affiliation><author><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K." last="Wenning">Gregor K. Wenning</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurological Research Laboratory, Department of Neurology, University Hospital of Innsbruck</s1>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14><country>Autriche</country>
</affiliation><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="2005">2005</date>
</imprint><seriesStmt><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
</seriesStmt><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Inclusion</term>
<term>Models</term>
<term>Multiple system atrophy</term>
<term>Nervous system diseases</term>
</keywords><keywords scheme="Pascal" xml:lang="fr"><term>Système nerveux pathologie</term>
<term>Atrophie multisystématisée</term>
<term>Modèle</term>
<term>Inclusion</term>
</keywords><front><div type="abstract" xml:lang="en">α-Synuclein represents the major constituent of oligodendroglial cytoplasmic inclusions, the hallmark lesion of multiple system atrophy (MSA), a progressive disorder that is associated with selective degenerative cell loss in basal ganglia, cerebellum, brainstem, and spinal cord. The role of abnormal α-synuclein aggregation in oligodendroglial cells is still obscure, in particular, whether α-synuclein might impair oligodendroglial and, secondarily, neuronal integrity of those cells in the diseased brain. In an attempt to answer some of these questions, we have developed an "in vitro model of MSA" by expressing the wild-type or C-terminally truncated form of α-synuclein in glial cell cultures. With this simplified system, we have demonstrated that α-synuclein significantly affects the survival of glia and its vulnerability to environmental stress, which might represent a major step in the pathogenesis of MSA.</div>
</front><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0>
</fA01><fA03 i2="1"><s0>Mov. disord.</s0>
</fA03><fA06><s3>SUP12</s3>
</fA06><fA08 i1="01" i2="1" l="ENG"><s1>In vitro models of multiple system atrophy</s1>
</fA08><fA09 i1="01" i2="1" l="ENG"><s1>Atypical Parkinsonian Disorders</s1>
</fA09><fA11 i1="01" i2="1"><s1>STEFANOVA (Nadia)</s1>
</fA11><fA11 i1="02" i2="1"><s1>REINDL (Markus)</s1>
</fA11><fA11 i1="03" i2="1"><s1>POEWE (Werner)</s1>
</fA11><fA11 i1="04" i2="1"><s1>WENNING (Gregor K.)</s1>
</fA11><fA12 i1="01" i2="1"><s1>POEWE (Werner)</s1>
<s9>ed.</s9>
</fA12><fA12 i1="02" i2="1"><s1>WENNING (Gregor K.)</s1>
<s9>ed.</s9>
</fA12><fA14 i1="01"><s1>Neurological Research Laboratory, Department of Neurology, University Hospital of Innsbruck</s1>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14><fA15 i1="01"><s1>Department of Neurology, Medical University Innsbruck</s1>
<s2>Innsbruck</s2>
<s3>AUT</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
</fA15><fA20><s2>S53-S56</s2>
</fA20><fA21><s1>2005</s1>
</fA21><fA23 i1="01"><s0>ENG</s0>
</fA23><fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000132714250080</s5>
</fA43><fA44><s0>0000</s0>
<s1>© 2005 INIST-CNRS. All rights reserved.</s1>
</fA44><fA45><s0>13 ref.</s0>
</fA45><fA47 i1="01" i2="1"><s0>05-0457543</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>α-Synuclein represents the major constituent of oligodendroglial cytoplasmic inclusions, the hallmark lesion of multiple system atrophy (MSA), a progressive disorder that is associated with selective degenerative cell loss in basal ganglia, cerebellum, brainstem, and spinal cord. The role of abnormal α-synuclein aggregation in oligodendroglial cells is still obscure, in particular, whether α-synuclein might impair oligodendroglial and, secondarily, neuronal integrity of those cells in the diseased brain. In an attempt to answer some of these questions, we have developed an "in vitro model of MSA" by expressing the wild-type or C-terminally truncated form of α-synuclein in glial cell cultures. With this simplified system, we have demonstrated that α-synuclein significantly affects the survival of glia and its vulnerability to environmental stress, which might represent a major step in the pathogenesis of MSA.</s0>
</fC01><fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02><fC02 i1="02" i2="X"><s0>002B17F</s0>
</fC02><fC02 i1="03" i2="X"><s0>002B17G</s0>
</fC02><fC03 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>01</s5>
</fC03><fC03 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>01</s5>
</fC03><fC03 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>01</s5>
</fC03><fC03 i1="02" i2="X" l="FRE"><s0>Atrophie multisystématisée</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03><fC03 i1="02" i2="X" l="ENG"><s0>Multiple system atrophy</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03><fC03 i1="02" i2="X" l="SPA"><s0>Atrofia multisistematizada</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03><fC03 i1="03" i2="X" l="FRE"><s0>Modèle</s0>
<s5>09</s5>
</fC03><fC03 i1="03" i2="X" l="ENG"><s0>Models</s0>
<s5>09</s5>
</fC03><fC03 i1="03" i2="X" l="SPA"><s0>Modelo</s0>
<s5>09</s5>
</fC03><fC03 i1="04" i2="X" l="FRE"><s0>Inclusion</s0>
<s5>10</s5>
</fC03><fC03 i1="04" i2="X" l="ENG"><s0>Inclusion</s0>
<s5>10</s5>
</fC03><fC03 i1="04" i2="X" l="SPA"><s0>Inclusión</s0>
<s5>10</s5>
</fC03><fN21><s1>318</s1>
</fN21><fN44 i1="01"><s1>OTO</s1>
</fN44><fN82><s1>OTO</s1>
</fN82><pR><fA30 i1="01" i2="1" l="ENG"><s1>Atypical Parkinsonian Disorders - From Protein Dysfunction to Therapeutic Intervention. International Meeting</s1>
<s3>Innsbruck AUT</s3>
<s4>2003-02-19</s4>
</fA30>
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 000F49 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Curation/biblio.hfd -nk 000F49 | 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:05-0457543
|texte= In vitro models of multiple system atrophy
}}
| 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 |  |
