Linked Life Data

15681812

Source:http://linkedlifedata.com/resource/pubmed/id/15681812

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2005-1-31
pubmed:abstractText
Although alpha-synuclein is a central player in the pathophysiology of the dopaminergic neurodegeneration that occurs in Parkinson's disease (PD), emerging results suggest that the fundamental property of the wild-type form of this protein may be one of neuroprotection, as it can inhibit apoptosis in response to various pro-apoptotic stimuli. Such properties may be lost by its familial PD-linked mutations upon alterations in its expression levels or clearance (overexpression of the gene, reduced protein degradation) or following exposure to certain neurotoxins. Moreover, converging observations suggest that a primary function for alpha-synuclein in dopaminergic neurons may be the regulation of dopamine content and tone at the synapse. In this paper, we review how, indeed, alpha-synuclein regulates both the synthesis of dopamine, its storage into vesicles, its release in the synapse, and its re-uptake into the dopaminergic neurons. We also show how disruption of these events, and of the neuroprotective effects of alpha-synuclein, can initiate the observed neurotoxicity of alpha-synuclein in dopaminergic neurons and the genesis of the degenerative processes associated with PD.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
1035
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
250-70
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
The role of alpha-synuclein in both neuroprotection and neurodegeneration.
pubmed:affiliation
Department of Pediatrics, Georgetown University, Washington, DC 20007, USA. sidhua@georgetown.edu
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural