THURSDAY, Aug. 23 (HealthDay News) -- Mice prone to developing Alzheimer disease develop fewer amyloid plaques and have less oxidative damage if they lack mitochondrial cytochrome c oxidase (COX) activity in neurons, according to a study published online Aug. 21 in the Proceedings of the National Academy of Sciences.
Carlos T. Moraes, Ph.D., and colleagues from the University of Miami removed COX function in post-mitotic neurons, particularly in the cerebral cortex and hippocampus, of mice that were prone to developing Alzheimer disease. The COX deficiency was age-dependent.
The researchers found that the mice lacking COX function had significantly fewer amyloid plaques in their brains, as well as reduced Aβ42 levels, β-secretase activity and oxidative damage. There was no increase in the production of reactive oxygen species from cells with partial COX activity.
"Collectively, our results suggest that, contrary to previous models, a defect in neuronal COX does not increase oxidative damage nor predispose for the formation of amyloidgenic amyloid precursor protein fragments," Moraes and colleagues conclude.
Abstract
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