Linked Life Data

14663012

Source:http://linkedlifedata.com/resource/pubmed/id/14663012

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11 Suppl 6
pubmed:dateCreated
2003-12-9
pubmed:abstractText
A remarkable convergence of epidemiologic and laboratory data has raised the possibility that caffeine reduces the risk of developing Parkinson's disease (PD) by preventing the degeneration of nigrostriatal dopaminergic neurons. The authors review the evidence that caffeine and more specific antagonists of the adenosine A2A receptor protect dopaminergic neurons in several toxin models of PD. Other studies demonstrating protection by A2A receptor inactivation in animal models of stroke, Huntington's disease, and Alzheimer's disease suggest a more global role of A2A receptors in neuronal injury and degeneration. Although the cellular and molecular mechanisms by which A2A receptors contribute to neuronal death are not yet established, several intriguing possibilities have emerged. Now with preliminary clinical data substantiating the antiparkinsonian symptomatic benefit of A2A receptor blockade, the prospects for a complementary neuroprotective benefit have enhanced the therapeutic potential of A2A antagonists in PD.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1526-632X
pubmed:author
pubmed:issnType
Electronic
pubmed:day
9
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S55-61
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Neuroprotection by caffeine and more specific A2A receptor antagonists in animal models of Parkinson's disease.
pubmed:affiliation
Department of Neurology, Massachusetts General Hospital, Boston, MA 02129, USA. michaels@helix.mgh.harvard.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't