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Aug 22, 2007

Inhibiting Gene Found to Reduce Amyloid Plaques

  • 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.



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Scientifically Studying Ecstasy

MDMA (commonly known as the empathogen “ecstasy”) is classified as a Schedule 1 drug, which is reserved for compounds with no accepted medical use and a high abuse potential. Two researchers from Stanford, however, call for a rigorous scientific exploration of MDMA's effects to identify precisely how the drug works, the data from which could be used to develop therapeutic compounds.

Do you agree that ecstasy should be studied for its potential therapeutic benefits?

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