Movement Disorders (revue)

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No Lewy pathology in monkeys with over 10 years of severe MPTP Parkinsonism

Identifieur interne : 002A43 ( Main/Merge ); précédent : 002A42; suivant : 002A44

No Lewy pathology in monkeys with over 10 years of severe MPTP Parkinsonism

Auteurs : Glenda Halliday [Australie] ; Maria Trinidad Herrero [Espagne] ; Karen Murphy [Australie] ; Heather Mccann [Australie] ; Francisco Ros-Bernal [Espagne] ; Carlos Barcia [Espagne] ; Hideo Mori [Japon] ; Francisco J. Blesa [Espagne] ; José A. Obeso [Espagne]

Source :

RBID : ISTEX:BA01BF2A4BF1B8D8E3448DBA2962402B2D51D6B5

English descriptors

Abstract

The recent knowledge that 10 years after transplantation surviving human fetal neurons adopt the histopathology of Parkinson's disease suggests that Lewy body formation takes a decade to achieve. To determine whether similar histopathology occurs in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐primate models over a similar timeframe, the brains of two adult monkeys made parkinsonian in their youth with intermittent injections of MPTP were studied. Despite substantial nigral degeneration and increased α‐synuclein immunoreactivity within surviving neurons, there was no evidence of Lewy body formation. This suggests that MPTP‐induced oxidative stress and inflammation per se are not sufficient for Lewy body formation, or Lewy bodies are human specific. © 2009 Movement Disorder Society

Url:
DOI: 10.1002/mds.22481

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ISTEX:BA01BF2A4BF1B8D8E3448DBA2962402B2D51D6B5

Le document en format XML

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<idno type="doi">10.1002/mds.22481</idno>
<idno type="RBID">pubmed:19526568</idno>
<idno type="pmid">19526568</idno>
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<analytic>
<title xml:lang="en">No Lewy pathology in monkeys with over 10 years of severe MPTP Parkinsonism.</title>
<author>
<name sortKey="Halliday, Glenda" sort="Halliday, Glenda" uniqKey="Halliday G" first="Glenda" last="Halliday">Glenda Halliday</name>
<affiliation wicri:level="3">
<nlm:affiliation>Prince of Wales Medical Research Institute and School of Medical Sciences, Faculty of Medicine University of New South Wales, Sydney, Australia. g.halliday@powmri.edu.au</nlm:affiliation>
<country xml:lang="fr">Australie</country>
<wicri:regionArea>Prince of Wales Medical Research Institute and School of Medical Sciences, Faculty of Medicine University of New South Wales, Sydney</wicri:regionArea>
<placeName>
<settlement type="city">Sydney</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Herrero, Maria Trinidad" sort="Herrero, Maria Trinidad" uniqKey="Herrero M" first="Maria Trinidad" last="Herrero">Maria Trinidad Herrero</name>
</author>
<author>
<name sortKey="Murphy, Karen" sort="Murphy, Karen" uniqKey="Murphy K" first="Karen" last="Murphy">Karen Murphy</name>
</author>
<author>
<name sortKey="Mccann, Heather" sort="Mccann, Heather" uniqKey="Mccann H" first="Heather" last="Mccann">Heather Mccann</name>
</author>
<author>
<name sortKey="Ros Bernal, Francisco" sort="Ros Bernal, Francisco" uniqKey="Ros Bernal F" first="Francisco" last="Ros-Bernal">Francisco Ros-Bernal</name>
</author>
<author>
<name sortKey="Barcia, Carlos" sort="Barcia, Carlos" uniqKey="Barcia C" first="Carlos" last="Barcia">Carlos Barcia</name>
</author>
<author>
<name sortKey="Mori, Hideo" sort="Mori, Hideo" uniqKey="Mori H" first="Hideo" last="Mori">Hideo Mori</name>
</author>
<author>
<name sortKey="Blesa, Francisco J" sort="Blesa, Francisco J" uniqKey="Blesa F" first="Francisco J" last="Blesa">Francisco J. Blesa</name>
</author>
<author>
<name sortKey="Obeso, Jose A" sort="Obeso, Jose A" uniqKey="Obeso J" first="José A" last="Obeso">José A. Obeso</name>
</author>
</analytic>
<series>
<title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
<idno type="eISSN">1531-8257</idno>
<imprint>
<date when="2009" type="published">2009</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Animals</term>
<term>Disease Models, Animal</term>
<term>Disease Progression</term>
<term>Lewy Bodies (pathology)</term>
<term>Longitudinal Studies</term>
<term>MPTP Poisoning (metabolism)</term>
<term>MPTP Poisoning (pathology)</term>
<term>Macaca fascicularis</term>
<term>Tyrosine 3-Monooxygenase (metabolism)</term>
<term>alpha-Synuclein (metabolism)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>Tyrosine 3-Monooxygenase</term>
<term>alpha-Synuclein</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>MPTP Poisoning</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en">
<term>Lewy Bodies</term>
<term>MPTP Poisoning</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Animals</term>
<term>Disease Models, Animal</term>
<term>Disease Progression</term>
<term>Longitudinal Studies</term>
<term>Macaca fascicularis</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">The recent knowledge that 10 years after transplantation surviving human fetal neurons adopt the histopathology of Parkinson's disease suggests that Lewy body formation takes a decade to achieve. To determine whether similar histopathology occurs in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-primate models over a similar timeframe, the brains of two adult monkeys made parkinsonian in their youth with intermittent injections of MPTP were studied. Despite substantial nigral degeneration and increased alpha-synuclein immunoreactivity within surviving neurons, there was no evidence of Lewy body formation. This suggests that MPTP-induced oxidative stress and inflammation per se are not sufficient for Lewy body formation, or Lewy bodies are human specific.</div>
</front>
</TEI>
</PubMed>
</double>
</record>

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