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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
1992-4-6
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pubmed:abstractText |
Mature cortical cultures, transiently deprived of glucose, developed slight neuronal damage that was exacerbated by exposure to a synthetic analog of the beta-amyloid protein deposited in the neuritic plaques of Alzheimer's disease. The non-competitive N-methyl-D-aspartate antagonist MK801 attenuated the injury-increasing effect of beta-amyloid protein implicating involvement of endogenous excitatory amino acids. These results suggest that beta-amyloid protein may accelerate neuronal degeneration in the presence of defective cerebral glucose metabolism which has been reported to occur in Alzheimer's disease.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0959-4965
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
2
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
763-5
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:1793819-Amyloid beta-Peptides,
pubmed-meshheading:1793819-Animals,
pubmed-meshheading:1793819-Cells, Cultured,
pubmed-meshheading:1793819-Cerebral Cortex,
pubmed-meshheading:1793819-Culture Media,
pubmed-meshheading:1793819-Dizocilpine Maleate,
pubmed-meshheading:1793819-Glucose,
pubmed-meshheading:1793819-L-Lactate Dehydrogenase,
pubmed-meshheading:1793819-Microscopy, Phase-Contrast,
pubmed-meshheading:1793819-N-Methylaspartate,
pubmed-meshheading:1793819-Neurons
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pubmed:year |
1991
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pubmed:articleTitle |
Beta-amyloid increases neuronal susceptibility to injury by glucose deprivation.
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pubmed:affiliation |
Department of Psychobiology, University of California Irvine 92715.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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