Ageing as a primary risk factor for Parkinson's disease: evidence from studies of non-human primates
Identifieur interne : 000402 ( Main/Exploration ); précédent : 000401; suivant : 000403Ageing as a primary risk factor for Parkinson's disease: evidence from studies of non-human primates
Auteurs : Timothy J. Collier [États-Unis] ; Nicholas M. Kanaan [États-Unis] ; Jeffrey H. Kordower [États-Unis]Source :
- Nature Reviews Neuroscience [ 1471-003X ] ; 2011-06.
Abstract
Ageing is the greatest risk factor for the development of Parkinson's disease. However, the current dogma holds that cellular mechanisms that are associated with ageing of midbrain dopamine neurons and those that are related to dopamine neuron degeneration in Parkinson's disease are unrelated. We propose, based on evidence from studies of non-human primates, that normal ageing and the degeneration of dopamine neurons in Parkinson's disease are linked by the same cellular mechanisms and, therefore, that markers of cellular risk factors accumulate with age in a pattern that mimics the pattern of degeneration observed in Parkinson's disease. We contend that ageing induces a pre-parkinsonian state, and that the cellular mechanisms of dopamine neuron demise during normal ageing are accelerated or exaggerated in Parkinson's disease through a combination of genetic and environmental factors.
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DOI: 10.1038/nrn3039
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Kordower</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:423B4A61DCA9F544119F61C9D00B7212B82D3342</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1038/nrn3039</idno><idno type="url">https://api.istex.fr/document/423B4A61DCA9F544119F61C9D00B7212B82D3342/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000389</idno><idno type="wicri:Area/Main/Curation">000336</idno><idno type="wicri:Area/Main/Exploration">000402</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Ageing as a primary risk factor for Parkinson's disease: evidence from studies of non-human primates</title><author><name sortKey="Collier, Timothy J" sort="Collier, Timothy J" uniqKey="Collier T" first="Timothy J." last="Collier">Timothy J. Collier</name><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Timothy J. Collier and Nicholas M. Kanaan are at the Division of Translational Science and Molecular Medicine, Michigan State University, Grand Rapids, Michigan 49503</wicri:regionArea><wicri:noRegion>Michigan 49503</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Timothy J. Collier is also at the Center of Excellence in Parkinson's Disease Research, Michigan State University, Grand Rapids, Michigan 49503</wicri:regionArea><wicri:noRegion>Michigan 49503</wicri:noRegion></affiliation><affiliation><wicri:noCountry code="no comma">T.J.C. and N.M.K. contributed equally to this work.</wicri:noCountry></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation></author><author><name sortKey="Kanaan, Nicholas M" sort="Kanaan, Nicholas M" uniqKey="Kanaan N" first="Nicholas M." last="Kanaan">Nicholas M. Kanaan</name><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Timothy J. Collier and Nicholas M. Kanaan are at the Division of Translational Science and Molecular Medicine, Michigan State University, Grand Rapids, Michigan 49503</wicri:regionArea><wicri:noRegion>Michigan 49503</wicri:noRegion></affiliation><affiliation><wicri:noCountry code="no comma">T.J.C. and N.M.K. contributed equally to this work.</wicri:noCountry></affiliation></author><author><name sortKey="Kordower, Jeffrey H" sort="Kordower, Jeffrey H" uniqKey="Kordower J" first="Jeffrey H." last="Kordower">Jeffrey H. Kordower</name><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Jeffrey H. Kordower is at the Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612</wicri:regionArea><wicri:noRegion>Illinois 60612</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Nature Reviews Neuroscience</title><idno type="ISSN">1471-003X</idno><idno type="eISSN">1471-0048</idno><imprint><publisher>Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.</publisher><date type="published" when="2011-06">2011-06</date><biblScope unit="volume">12</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="359">359</biblScope><biblScope unit="page" to="366">366</biblScope></imprint><idno type="ISSN">1471-003X</idno></series><idno type="istex">423B4A61DCA9F544119F61C9D00B7212B82D3342</idno><idno type="DOI">10.1038/nrn3039</idno><idno type="ArticleID">nrn3039</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1471-003X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="eng">Ageing is the greatest risk factor for the development of Parkinson's disease. However, the current dogma holds that cellular mechanisms that are associated with ageing of midbrain dopamine neurons and those that are related to dopamine neuron degeneration in Parkinson's disease are unrelated. We propose, based on evidence from studies of non-human primates, that normal ageing and the degeneration of dopamine neurons in Parkinson's disease are linked by the same cellular mechanisms and, therefore, that markers of cellular risk factors accumulate with age in a pattern that mimics the pattern of degeneration observed in Parkinson's disease. We contend that ageing induces a pre-parkinsonian state, and that the cellular mechanisms of dopamine neuron demise during normal ageing are accelerated or exaggerated in Parkinson's disease through a combination of genetic and environmental factors.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Collier, Timothy J" sort="Collier, Timothy J" uniqKey="Collier T" first="Timothy J." last="Collier">Timothy J. Collier</name></noRegion><name sortKey="Collier, Timothy J" sort="Collier, Timothy J" uniqKey="Collier T" first="Timothy J." last="Collier">Timothy J. Collier</name><name sortKey="Collier, Timothy J" sort="Collier, Timothy J" uniqKey="Collier T" first="Timothy J." last="Collier">Timothy J. Collier</name><name sortKey="Kanaan, Nicholas M" sort="Kanaan, Nicholas M" uniqKey="Kanaan N" first="Nicholas M." last="Kanaan">Nicholas M. Kanaan</name><name sortKey="Kordower, Jeffrey H" sort="Kordower, Jeffrey H" uniqKey="Kordower J" first="Jeffrey H." last="Kordower">Jeffrey H. Kordower</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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