Linked Life Data

10661495

Source:http://linkedlifedata.com/resource/pubmed/id/10661495

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-2-22
pubmed:abstractText
Zinc and copper are endogenous transition metals that can be synaptically released during neuronal activity. Synaptically released zinc and copper probably function to modulate neuronal excitability under normal conditions. However, zinc and copper also can be neurotoxic, and it has been proposed that they may contribute to the neuropathology associated with a variety of conditions, such as Alzheimer's disease, stroke, and seizures. Recently, we demonstrated that carnosine, a dipeptide expressed in glial cells throughout the brain as well as in neuronal pathways of the visual and olfactory systems, can modulate the effects of zinc and copper on neuronal excitability. This result led us to hypothesize that carnosine may modulate the neurotoxic effects of zinc and copper as well. Our results demonstrate that carnosine can rescue neurons from zinc- and copper-mediated neurotoxicity and suggest that one function of carnosine may be as an endogenous neuroprotective agent.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
852
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
56-61
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Endogenous mechanisms of neuroprotection: role of zinc, copper, and carnosine.
pubmed:affiliation
Biomedical Research Facility, Department of Biological Science, Florida State University, Tallahassee 32306-4340, USA. horning@neuro.fsu.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.