Source:http://linkedlifedata.com/resource/pubmed/id/16006134
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2005-11-21
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pubmed:abstractText |
Changes in the expression of alpha-synuclein are likely to underlie its normal function as well as its role in pathological processes. The relationship between toxic injury and alpha-synuclein expression was assessed in the substantia nigra of squirrel monkeys treated with a single injection of MPTP and sacrificed 1 week or 1 month later. At 1 week, when stereological cell counting revealed only a small decrease (-10%) in the number of dopaminergic neurons, alpha-synuclein mRNA and protein were markedly enhanced. Increased alpha-synuclein immunoreactivity was evident at the level of neuronal fibers whereas nigral cell bodies were devoid of detectable protein. At 1 month post-MPTP, neuronal loss rose to 40%. Both alpha-synuclein mRNA and protein remained elevated but, noticeably, a robust alpha-synuclein immunoreactivity characterized a significant number of cell bodies. Neuromelanin granules are hallmarks of dopaminergic neurons in primates. Therefore, the number of alpha-synuclein-positive cells that also contained neuromelanin was counted throughout the substantia nigra. At 1 month, the vast majority of alpha-synuclein-immunoreactive neurons contained neuromelanin, and approximately 80% of the dopaminergic cell bodies that survived MPTP toxicity stained positive for alpha-synuclein. The results indicate that a single toxic insult is capable of inducing a sustained alpha-synuclein up-regulation in the primate brain. They support a direct relationship between neuronal injury and enhanced alpha-synuclein expression, and suggest that protein elevation within cell bodies may be a late feature of neurons that have endured a toxic stress.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0969-9961
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
20
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
898-906
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:16006134-Animals,
pubmed-meshheading:16006134-Cell Count,
pubmed-meshheading:16006134-Cell Death,
pubmed-meshheading:16006134-Disease Models, Animal,
pubmed-meshheading:16006134-Dopamine,
pubmed-meshheading:16006134-Female,
pubmed-meshheading:16006134-Melanins,
pubmed-meshheading:16006134-Nerve Degeneration,
pubmed-meshheading:16006134-Neurons,
pubmed-meshheading:16006134-Oxidative Stress,
pubmed-meshheading:16006134-Parkinsonian Disorders,
pubmed-meshheading:16006134-RNA, Messenger,
pubmed-meshheading:16006134-Saimiri,
pubmed-meshheading:16006134-Substantia Nigra,
pubmed-meshheading:16006134-Up-Regulation,
pubmed-meshheading:16006134-alpha-Synuclein
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pubmed:year |
2005
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pubmed:articleTitle |
Alpha-synuclein expression in the substantia nigra of MPTP-lesioned non-human primates.
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pubmed:affiliation |
The Parkinson's Institute, 1170 Morse Avenue, Sunnyvale, California 94089, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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