Beta-amyloid increases neuronal susceptibility to injury by glucose deprivation.
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.
Copani
A
A
Department of Psychobiology, University of California Irvine 92715.
Koh
J Y
JY
Cotman
C W
CW
D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000818:Animals; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism; D003470:Culture Media; D016291:Dizocilpine Maleate / Q000494:pharmacology; D005947:Glucose / Q000172:deficiency*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008858:Microscopy, Phase-Contrast; D016202:N-Methylaspartate / Q000037:antagonists & inhibitors; D009474:Neurons / Q000378:metabolism* / Q000473:pathology
D016229:Amyloid beta-Peptides; D003470:Culture Media; D016202:N-Methylaspartate; D016291:Dizocilpine Maleate; D007770:L-Lactate Dehydrogenase; D005947:Glucose