Serveur d'exploration sur la maladie de Parkinson

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.

Etiology and pathogenesis of Parkinson's disease

Identifieur interne : 000324 ( Main/Exploration ); précédent : 000323; suivant : 000325

Etiology and pathogenesis of Parkinson's disease

Auteurs : Anthony H. Schapira [Royaume-Uni] ; Peter Jenner [Royaume-Uni]

Source :

RBID : ISTEX:883462E872938F8DD373037D22B85EE75A857F71

English descriptors

Abstract

The past 25 years have seen a major expansion of knowledge concerning the cause of Parkinson's disease provided by an understanding of environmental and genetic factors that underlie the loss of nigral dopaminergic neurons. Based on the actions of toxins, postmortem investigations, and gene defects responsible for familial Parkinson's disease, there is now a general consensus about the mechanisms of cell death that contribute to neuronal loss in Parkinson's disease. Mitochondrial dysfunction, oxidative stress, altered protein handling, and inflammatory change are considered to lead to cell dysfunction and death by apoptosis or autophagy. Ageing is the single most important risk factor for Parkinson's disease, and the biochemical changes that are a consequence of aging amplify these abnormalities in Parkinson's disease brain. What remains to be determined is the combination and sequence of events leading to cell death and whether this is identical in all brain regions where pathology occurs and in all individuals with Parkinson's disease. Focusing on those events that characterize Parkinson's disease, namely, mitochondrial dysfunction and Lewy body formation, may be the key to further advancing the understanding of pathogenesis and to taking these mechanisms forward as a means of defining targets for neuroprotection. © 2011 Movement Disorder Society

Url:
DOI: 10.1002/mds.23732


Affiliations:


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


Le document en format XML

<record>
<TEI wicri:istexFullTextTei="biblStruct">
<teiHeader>
<fileDesc>
<titleStmt>
<title xml:lang="en">Etiology and pathogenesis of Parkinson's disease</title>
<author>
<name sortKey="Schapira, Anthony H" sort="Schapira, Anthony H" uniqKey="Schapira A" first="Anthony H." last="Schapira">Anthony H. Schapira</name>
</author>
<author>
<name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:883462E872938F8DD373037D22B85EE75A857F71</idno>
<date when="2011" year="2011">2011</date>
<idno type="doi">10.1002/mds.23732</idno>
<idno type="url">https://api.istex.fr/document/883462E872938F8DD373037D22B85EE75A857F71/fulltext/pdf</idno>
<idno type="wicri:Area/Main/Corpus">000573</idno>
<idno type="wicri:Area/Main/Curation">000498</idno>
<idno type="wicri:Area/Main/Exploration">000324</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title level="a" type="main" xml:lang="en">Etiology and pathogenesis of Parkinson's disease</title>
<author>
<name sortKey="Schapira, Anthony H" sort="Schapira, Anthony H" uniqKey="Schapira A" first="Anthony H." last="Schapira">Anthony H. Schapira</name>
<affiliation wicri:level="3">
<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Department of Clinical Neurosciences, Institute of Neurology, University College, London</wicri:regionArea>
<placeName>
<settlement type="city">Londres</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Grand Londres</region>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name>
<affiliation wicri:level="3">
<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Neurodegenerative Diseases Research Centre, Institute of Pharmaceutical Sciences, School of Biomedical Sciences, King's College, London</wicri:regionArea>
<placeName>
<settlement type="city">Londres</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Grand Londres</region>
</placeName>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series>
<title level="j">Movement Disorders</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="2011-05">2011-05</date>
<biblScope unit="volume">26</biblScope>
<biblScope unit="issue">6</biblScope>
<biblScope unit="page" from="1049">1049</biblScope>
<biblScope unit="page" to="1055">1055</biblScope>
</imprint>
<idno type="ISSN">0885-3185</idno>
</series>
<idno type="istex">883462E872938F8DD373037D22B85EE75A857F71</idno>
<idno type="DOI">10.1002/mds.23732</idno>
<idno type="ArticleID">MDS23732</idno>
</biblStruct>
</sourceDesc>
<seriesStmt>
<idno type="ISSN">0885-3185</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Parkinson's disease</term>
<term>environment</term>
<term>etiology</term>
<term>genetics</term>
<term>mitochondria</term>
<term>oxidative stress</term>
<term>pathogenesis</term>
</keywords>
</textClass>
<langUsage>
<language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">The past 25 years have seen a major expansion of knowledge concerning the cause of Parkinson's disease provided by an understanding of environmental and genetic factors that underlie the loss of nigral dopaminergic neurons. Based on the actions of toxins, postmortem investigations, and gene defects responsible for familial Parkinson's disease, there is now a general consensus about the mechanisms of cell death that contribute to neuronal loss in Parkinson's disease. Mitochondrial dysfunction, oxidative stress, altered protein handling, and inflammatory change are considered to lead to cell dysfunction and death by apoptosis or autophagy. Ageing is the single most important risk factor for Parkinson's disease, and the biochemical changes that are a consequence of aging amplify these abnormalities in Parkinson's disease brain. What remains to be determined is the combination and sequence of events leading to cell death and whether this is identical in all brain regions where pathology occurs and in all individuals with Parkinson's disease. Focusing on those events that characterize Parkinson's disease, namely, mitochondrial dysfunction and Lewy body formation, may be the key to further advancing the understanding of pathogenesis and to taking these mechanisms forward as a means of defining targets for neuroprotection. © 2011 Movement Disorder Society</div>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>Royaume-Uni</li>
</country>
<region>
<li>Angleterre</li>
<li>Grand Londres</li>
</region>
<settlement>
<li>Londres</li>
</settlement>
</list>
<tree>
<country name="Royaume-Uni">
<region name="Angleterre">
<name sortKey="Schapira, Anthony H" sort="Schapira, Anthony H" uniqKey="Schapira A" first="Anthony H." last="Schapira">Anthony H. Schapira</name>
</region>
<name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000324 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000324 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Sante
   |area=    ParkinsonV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     ISTEX:883462E872938F8DD373037D22B85EE75A857F71
   |texte=   Etiology and pathogenesis of Parkinson's disease
}}

Wicri

This area was generated with Dilib version V0.6.23.
Data generation: Sun Jul 3 18:06:51 2016. Site generation: Wed Mar 6 18:46:03 2024