Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-4-1
pubmed:abstractText
Glutamate neurotoxicity may be an underlying pathological mechanism contributing to neuronal cell loss in a variety of conditions including Alzheimer's disease (AD). In this study, we examined whether the beta-amyloid protein found in the neuritic plaques of AD alters the susceptibility of neurons to excitotoxic damage. While mature cortical neurons exposed to beta-amyloid protein for 2-4 days did not appear to be damaged, their vulnerability to low-intensity exposure to glutamate, N-methyl-D-aspartate, and kainate increased, suggesting that this mechanism may contribute to the neurodegeneration seen in AD.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
19
pubmed:volume
533
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
315-20
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Beta-amyloid protein increases the vulnerability of cultured cortical neurons to excitotoxic damage.
pubmed:affiliation
Department of Psychobiology, University of California, Irvine 92717.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.