pubmed-article:18157654 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18157654 | lifeskim:mentions | umls-concept:C0030567 | lld:lifeskim |
pubmed-article:18157654 | lifeskim:mentions | umls-concept:C0521119 | lld:lifeskim |
pubmed-article:18157654 | lifeskim:mentions | umls-concept:C0285890 | lld:lifeskim |
pubmed-article:18157654 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:18157654 | lifeskim:mentions | umls-concept:C0439659 | lld:lifeskim |
pubmed-article:18157654 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:18157654 | pubmed:dateCreated | 2007-12-24 | lld:pubmed |
pubmed-article:18157654 | pubmed:abstractText | Misfolding and abnormal aggregation of the neuronal protein alpha-synuclein has been implicated in the pathogenesis of Parkinson's disease and related neurological disorders, such as dementia with Lewy bodies. alpha-synuclein is a conventional cytosolic protein and is thought to exert its pathogenic function exclusively in the neuronal cytoplasm in a cell-autonomous manner. However, the current model is being challenged by a series of new observations that demonstrate the presence of alpha-synuclein and its aggregated forms in the extracellular fluid both in vivo and in vitro. Extracellular alpha-synuclein appears to be delivered by unconventional exocytosis of intravesicular alpha-synuclein, although the exact mechanism has not been characterized. Compared to the cytosolic alpha-synuclein, intravesicular alpha-synuclein is prone to aggregation and the potential source of extracellular aggregates. A number of tissue culture studies suggest that exposure to extracellular alpha-synuclein aggregates induces microglial activation, release of pro-inflammatory cytokines from astrocytes, and neurotoxicity. Thus, exocytosis of alpha-synuclein may be an important mechanism for amplifying and spreading degenerative changes from a small group of cells to its surrounding tissues, and it potentially provides therapeutic targets for halting the progression of the disease. | lld:pubmed |
pubmed-article:18157654 | pubmed:language | eng | lld:pubmed |
pubmed-article:18157654 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18157654 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18157654 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18157654 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18157654 | pubmed:issn | 0895-8696 | lld:pubmed |
pubmed-article:18157654 | pubmed:author | pubmed-author:LeeSeung-JaeS... | lld:pubmed |
pubmed-article:18157654 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:18157654 | pubmed:volume | 34 | lld:pubmed |
pubmed-article:18157654 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18157654 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18157654 | pubmed:pagination | 17-22 | lld:pubmed |
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pubmed-article:18157654 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18157654 | pubmed:articleTitle | Origins and effects of extracellular alpha-synuclein: implications in Parkinson's disease. | lld:pubmed |
pubmed-article:18157654 | pubmed:affiliation | Center for Geriatric Neuroscience Research, Institute of Biomedical Science and Technology, Department of Biomedical Science and Technology, Konkuk University, Seoul, Republic of Korea. sjlee@konkuk.ac.kr | lld:pubmed |
pubmed-article:18157654 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18157654 | pubmed:publicationType | Review | lld:pubmed |
pubmed-article:18157654 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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