La maladie de Parkinson au Canada (serveur d'exploration)

Attention, ce site est en cours de développement !
Attention, site généré par des moyens informatiques à partir de corpus bruts.
Les informations ne sont donc pas validées.

Parkinson disease, 10 years after its genetic revolution : Multiple clues to a complex disorder

Identifieur interne : 000630 ( PascalFrancis/Curation ); précédent : 000629; suivant : 000631

Parkinson disease, 10 years after its genetic revolution : Multiple clues to a complex disorder

Auteurs : Christine Klein [Allemagne] ; Michael G. Schlossmacher [Canada]

Source :

RBID : Pascal:08-0043337

Descripteurs français

English descriptors

Abstract

Over the last 10 years, an unprecedented number of scientific reports have been published that relate to the pathogenesis of parkinsonism. Since the discovery in 1997 of the first heritable form of parkinsonism that could be linked to a mutation in a single gene, SNCA, many more genetic leads have followed (Parkin, DJ-1, PINK1, LRRK2, to name a few); these have provided us with many molecular clues to better explore the etiology of parkinsonism and have led to the dismantling of many previously held dogmas about Parkinson disease (PD). Epidemiologic studies have delineated an array of environmental modulators of susceptibility to parkinsonism, which can now be examined in the context of gene expression. Furthermore, in vivo imaging data and postmortem results have generated concepts that greatly expanded our appreciation for the phenotypic spectrum of parkinsonism from its presymptomatic to advanced stages. With this plethora of new information emerged the picture of a complex syndrome that raises many questions: How many forms of classic parkinsonism/Parkinson disease(s) are there? Where does the disease begin? What causes late-onset, "idiopathic" PD? What are the caveats related to genetic testing? What is the role of Lewy bodies? What will be the best disease model to accommodate the now known genetic and environmental contributors to parkinsonism? What will be the ideal markers and targets for earlier diagnosis and cause-directed therapy? In the following article we highlight some of the burning issues surrounding the understanding of classic parkinsonism, a complex puzzle of genes, environment, and an aging host.
pA  
A01 01  1    @0 0028-3878
A02 01      @0 NEURAI
A03   1    @0 Neurology
A05       @2 69
A06       @2 22
A08 01  1  ENG  @1 Parkinson disease, 10 years after its genetic revolution : Multiple clues to a complex disorder
A11 01  1    @1 KLEIN (Christine)
A11 02  1    @1 SCHLOSSMACHER (Michael G.)
A14 01      @1 Department of Neurology University of Lübeck @3 DEU @Z 1 aut.
A14 02      @1 OHRI-Division of Neuroscience University of Ottawa @2 Ontario @3 CAN @Z 2 aut.
A20       @1 2093-2104
A21       @1 2007
A23 01      @0 ENG
A43 01      @1 INIST @2 6345 @5 354000174428650100
A44       @0 0000 @1 © 2008 INIST-CNRS. All rights reserved.
A45       @0 144 ref.
A47 01  1    @0 08-0043337
A60       @1 P
A61       @0 A
A64 01  1    @0 Neurology
A66 01      @0 USA
C01 01    ENG  @0 Over the last 10 years, an unprecedented number of scientific reports have been published that relate to the pathogenesis of parkinsonism. Since the discovery in 1997 of the first heritable form of parkinsonism that could be linked to a mutation in a single gene, SNCA, many more genetic leads have followed (Parkin, DJ-1, PINK1, LRRK2, to name a few); these have provided us with many molecular clues to better explore the etiology of parkinsonism and have led to the dismantling of many previously held dogmas about Parkinson disease (PD). Epidemiologic studies have delineated an array of environmental modulators of susceptibility to parkinsonism, which can now be examined in the context of gene expression. Furthermore, in vivo imaging data and postmortem results have generated concepts that greatly expanded our appreciation for the phenotypic spectrum of parkinsonism from its presymptomatic to advanced stages. With this plethora of new information emerged the picture of a complex syndrome that raises many questions: How many forms of classic parkinsonism/Parkinson disease(s) are there? Where does the disease begin? What causes late-onset, "idiopathic" PD? What are the caveats related to genetic testing? What is the role of Lewy bodies? What will be the best disease model to accommodate the now known genetic and environmental contributors to parkinsonism? What will be the ideal markers and targets for earlier diagnosis and cause-directed therapy? In the following article we highlight some of the burning issues surrounding the understanding of classic parkinsonism, a complex puzzle of genes, environment, and an aging host.
C02 01  X    @0 002B17
C02 02  X    @0 002B17F
C02 03  X    @0 002B17G
C03 01  X  FRE  @0 Pathologie du système nerveux @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 Maladie de Parkinson @2 NM @5 02
C03 02  X  ENG  @0 Parkinson disease @2 NM @5 02
C03 02  X  SPA  @0 Parkinson enfermedad @2 NM @5 02
C03 03  X  FRE  @0 Maladie héréditaire @5 09
C03 03  X  ENG  @0 Genetic disease @5 09
C03 03  X  SPA  @0 Enfermedad hereditaria @5 09
C07 01  X  FRE  @0 Pathologie de l'encéphale @5 37
C07 01  X  ENG  @0 Cerebral disorder @5 37
C07 01  X  SPA  @0 Encéfalo patología @5 37
C07 02  X  FRE  @0 Syndrome extrapyramidal @5 38
C07 02  X  ENG  @0 Extrapyramidal syndrome @5 38
C07 02  X  SPA  @0 Extrapiramidal síndrome @5 38
C07 03  X  FRE  @0 Maladie dégénérative @5 39
C07 03  X  ENG  @0 Degenerative disease @5 39
C07 03  X  SPA  @0 Enfermedad degenerativa @5 39
C07 04  X  FRE  @0 Pathologie du système nerveux central @5 40
C07 04  X  ENG  @0 Central nervous system disease @5 40
C07 04  X  SPA  @0 Sistema nervosio central patología @5 40
N21       @1 021
N44 01      @1 OTO
N82       @1 OTO

Links toward previous steps (curation, corpus...)


Links to Exploration step

Pascal:08-0043337

Le document en format XML

<record>
<TEI>
<teiHeader>
<fileDesc>
<titleStmt>
<title xml:lang="en" level="a">Parkinson disease, 10 years after its genetic revolution : Multiple clues to a complex disorder</title>
<author>
<name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name>
<affiliation wicri:level="1">
<inist:fA14 i1="01">
<s1>Department of Neurology University of Lübeck</s1>
<s3>DEU</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
<country>Allemagne</country>
</affiliation>
</author>
<author>
<name sortKey="Schlossmacher, Michael G" sort="Schlossmacher, Michael G" uniqKey="Schlossmacher M" first="Michael G." last="Schlossmacher">Michael G. Schlossmacher</name>
<affiliation wicri:level="1">
<inist:fA14 i1="02">
<s1>OHRI-Division of Neuroscience University of Ottawa</s1>
<s2>Ontario</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
</inist:fA14>
<country>Canada</country>
</affiliation>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">INIST</idno>
<idno type="inist">08-0043337</idno>
<date when="2007">2007</date>
<idno type="stanalyst">PASCAL 08-0043337 INIST</idno>
<idno type="RBID">Pascal:08-0043337</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000680</idno>
<idno type="wicri:Area/PascalFrancis/Curation">000630</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title xml:lang="en" level="a">Parkinson disease, 10 years after its genetic revolution : Multiple clues to a complex disorder</title>
<author>
<name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name>
<affiliation wicri:level="1">
<inist:fA14 i1="01">
<s1>Department of Neurology University of Lübeck</s1>
<s3>DEU</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
<country>Allemagne</country>
</affiliation>
</author>
<author>
<name sortKey="Schlossmacher, Michael G" sort="Schlossmacher, Michael G" uniqKey="Schlossmacher M" first="Michael G." last="Schlossmacher">Michael G. Schlossmacher</name>
<affiliation wicri:level="1">
<inist:fA14 i1="02">
<s1>OHRI-Division of Neuroscience University of Ottawa</s1>
<s2>Ontario</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
</inist:fA14>
<country>Canada</country>
</affiliation>
</author>
</analytic>
<series>
<title level="j" type="main">Neurology</title>
<title level="j" type="abbreviated">Neurology</title>
<idno type="ISSN">0028-3878</idno>
<imprint>
<date when="2007">2007</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt>
<title level="j" type="main">Neurology</title>
<title level="j" type="abbreviated">Neurology</title>
<idno type="ISSN">0028-3878</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Genetic disease</term>
<term>Nervous system diseases</term>
<term>Parkinson disease</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Pathologie du système nerveux</term>
<term>Maladie de Parkinson</term>
<term>Maladie héréditaire</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Over the last 10 years, an unprecedented number of scientific reports have been published that relate to the pathogenesis of parkinsonism. Since the discovery in 1997 of the first heritable form of parkinsonism that could be linked to a mutation in a single gene, SNCA, many more genetic leads have followed (Parkin, DJ-1, PINK1, LRRK2, to name a few); these have provided us with many molecular clues to better explore the etiology of parkinsonism and have led to the dismantling of many previously held dogmas about Parkinson disease (PD). Epidemiologic studies have delineated an array of environmental modulators of susceptibility to parkinsonism, which can now be examined in the context of gene expression. Furthermore, in vivo imaging data and postmortem results have generated concepts that greatly expanded our appreciation for the phenotypic spectrum of parkinsonism from its presymptomatic to advanced stages. With this plethora of new information emerged the picture of a complex syndrome that raises many questions: How many forms of classic parkinsonism/Parkinson disease(s) are there? Where does the disease begin? What causes late-onset, "idiopathic" PD? What are the caveats related to genetic testing? What is the role of Lewy bodies? What will be the best disease model to accommodate the now known genetic and environmental contributors to parkinsonism? What will be the ideal markers and targets for earlier diagnosis and cause-directed therapy? In the following article we highlight some of the burning issues surrounding the understanding of classic parkinsonism, a complex puzzle of genes, environment, and an aging host.</div>
</front>
</TEI>
<inist>
<standard h6="B">
<pA>
<fA01 i1="01" i2="1">
<s0>0028-3878</s0>
</fA01>
<fA02 i1="01">
<s0>NEURAI</s0>
</fA02>
<fA03 i2="1">
<s0>Neurology</s0>
</fA03>
<fA05>
<s2>69</s2>
</fA05>
<fA06>
<s2>22</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG">
<s1>Parkinson disease, 10 years after its genetic revolution : Multiple clues to a complex disorder</s1>
</fA08>
<fA11 i1="01" i2="1">
<s1>KLEIN (Christine)</s1>
</fA11>
<fA11 i1="02" i2="1">
<s1>SCHLOSSMACHER (Michael G.)</s1>
</fA11>
<fA14 i1="01">
<s1>Department of Neurology University of Lübeck</s1>
<s3>DEU</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="02">
<s1>OHRI-Division of Neuroscience University of Ottawa</s1>
<s2>Ontario</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA20>
<s1>2093-2104</s1>
</fA20>
<fA21>
<s1>2007</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>6345</s2>
<s5>354000174428650100</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2008 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>144 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>08-0043337</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Neurology</s0>
</fA64>
<fA66 i1="01">
<s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>Over the last 10 years, an unprecedented number of scientific reports have been published that relate to the pathogenesis of parkinsonism. Since the discovery in 1997 of the first heritable form of parkinsonism that could be linked to a mutation in a single gene, SNCA, many more genetic leads have followed (Parkin, DJ-1, PINK1, LRRK2, to name a few); these have provided us with many molecular clues to better explore the etiology of parkinsonism and have led to the dismantling of many previously held dogmas about Parkinson disease (PD). Epidemiologic studies have delineated an array of environmental modulators of susceptibility to parkinsonism, which can now be examined in the context of gene expression. Furthermore, in vivo imaging data and postmortem results have generated concepts that greatly expanded our appreciation for the phenotypic spectrum of parkinsonism from its presymptomatic to advanced stages. With this plethora of new information emerged the picture of a complex syndrome that raises many questions: How many forms of classic parkinsonism/Parkinson disease(s) are there? Where does the disease begin? What causes late-onset, "idiopathic" PD? What are the caveats related to genetic testing? What is the role of Lewy bodies? What will be the best disease model to accommodate the now known genetic and environmental contributors to parkinsonism? What will be the ideal markers and targets for earlier diagnosis and cause-directed therapy? In the following article we highlight some of the burning issues surrounding the understanding of classic parkinsonism, a complex puzzle of genes, environment, and an aging host.</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>Pathologie du système nerveux</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>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Maladie héréditaire</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Genetic disease</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Enfermedad hereditaria</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>021</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/PascalFrancis/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000630 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Curation/biblio.hfd -nk 000630 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Canada
   |area=    ParkinsonCanadaV1
   |flux=    PascalFrancis
   |étape=   Curation
   |type=    RBID
   |clé=     Pascal:08-0043337
   |texte=   Parkinson disease, 10 years after its genetic revolution : Multiple clues to a complex disorder
}}

Wicri

This area was generated with Dilib version V0.6.29.
Data generation: Thu May 4 22:20:19 2017. Site generation: Fri Dec 23 23:17:26 2022