Cytochrome Oxidase Inhibition: A Novel Animal Model of Alzheimer's Disease
Digital Object Identifier (DOI)
A profound decrease in activity of the mitochondrial enzyme cytochrome oxidase in blood platelets is a recently identified concomitant of Alzheimer's disease (AD). We investigated a possible pathogenic link between this finding and the symptoms of AD by mimicking this mitochondrial enzyme deficiency in rats. Rats were infused chronically with a selective inhibitor of cytochrome oxidase, sodium azide, or with saline delivered via subcutaneously implanted osmotic minipumps. The azide treatment impaired both spatial and nonspatial learning. Further, the azide treatment inhibited a low-threshold form of hippocampal long-term potentiation, primed burst potentiation. The behavioral deficits were not secondary to a sensory or motor impairment. Thus, chronic azide treatment of rats models some characteristics of AD.
Was this content written or created while at USF?
Citation / Publisher Attribution
The Journal of Geriatric Psychiatry and Neurology, v. 5, issue 2, p. 93-101
Scholar Commons Citation
Bennett, M. Catherine; Diamond, David M.; Stryker, Stacy L.; Parks, Janice K.; and Parks, W. Davis, "Cytochrome Oxidase Inhibition: A Novel Animal Model of Alzheimer's Disease" (1992). Psychology Faculty Publications. 1299.