Mice lacking COX10 showed reduced A-beta-42 levels, beta-secretase activity, and oxidative damage.
Inhibition of the mitochondrial cytochrome c oxidase (COX) gene is asssociated to a slowing in the deposition of amyloid plaques in the brain, report scientists at the University of Miami Miller School of Medicine.
Previous research had linked genetic defects in COX with Alzheimer’s disease. In the current study, the team knocked out the activity of the COX10 gene in the cerebral cortex and hippocampus regions of mice and then examined them to determine how the gene impacted the course of Alzheimer’s.
Contrary to their expectations, the investigators say, COX10 knockout mice exhibited significantly fewer amyloid plaques in their brains compared with the COX-competent transgenic mice.
The scientists found that eliminating the activity of the gene in the cortex and hippocampus was accompanied by a reduction in A-beta-42 levels, beta-secretase activity, which is critical for forming the amyloid plaques, and oxidative damage.
The research team states 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.
The study was published in August 21 issue of Proceedings of the National Academy of Sciences.