Source:http://linkedlifedata.com/resource/pubmed/id/19429081
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2009-5-11
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pubmed:abstractText |
alpha-Synuclein (alpha-Syn) abnormality and mitochondrial deficiency are two major changes in the brain of patients with Parkinson's disease (PD). A link between alpha-Syn and mitochondria in PD has been demonstrated by a recent study showing that accumulation of alpha-Syn in the mitochondria from the PD-vulnerable brain regions was associated with decreased complex I activity of these mitochondria. In this study, we examined the normal expressions of alpha-Syn in mitochondria from different regions of the rat brain. We showed that alpha-Syn was highly expressed in the mitochondria in olfactory bulb, hippocampus, striatum, and thalamus, where the cytosolic alpha-Syn was also rich. However, the cerebral cortex and cerebellum were two exceptions, which contained rich cytosolic alpha-Syn but very low or even undetectable levels of mitochondrial alpha-Syn. The close quantitative association between mitochondrial and cytosolic alpha-Syn in most brain regions, suggests that the concentration of cytosolic alpha-Syn may determine the amount of alpha-Syn in mitochondria. This is partially supported by the in vitro experiment showing that incubation of alpha-Syn with endogenous alpha-Syn-undetectable cerebellar mitochondria caused a dose-dependent transport of alpha-Syn to the mitochondria. Moreover, we found that the inhibitory effect of alpha-Syn on complex I activity of mitochondrial respiratory chain was also dose-dependent. These results suggest that alpha-Syn in mitochondria is differentially expressed in different brain regions and the background levels of mitochondrial alpha-Syn may be a potential factor affecting mitochondrial function and predisposing some neurons to degeneration.
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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 |
May
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pubmed:issn |
1872-7972
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
454
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
187-92
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pubmed:meshHeading |
pubmed-meshheading:19429081-Animals,
pubmed-meshheading:19429081-Blotting, Western,
pubmed-meshheading:19429081-Brain,
pubmed-meshheading:19429081-Cytoplasm,
pubmed-meshheading:19429081-Down-Regulation,
pubmed-meshheading:19429081-Electron Transport Complex I,
pubmed-meshheading:19429081-Male,
pubmed-meshheading:19429081-Mitochondria,
pubmed-meshheading:19429081-Protein Transport,
pubmed-meshheading:19429081-Rats,
pubmed-meshheading:19429081-Rats, Wistar,
pubmed-meshheading:19429081-alpha-Synuclein
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pubmed:year |
2009
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pubmed:articleTitle |
alpha-Synuclein is differentially expressed in mitochondria from different rat brain regions and dose-dependently down-regulates complex I activity.
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pubmed:affiliation |
Department of Neurobiology and Sino-Japan Joint Laboratory for Neurodegenerative Diseases, Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Xuanwu Hospital of China Capital Medical University, Beijing, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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