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Transgenomic Obtains Exclusive License to Mitochondrial DNA Damage Detection Technology
Date:12/4/2008

hed more than 30 papers using this technology to follow damage and repair in mitochondrial and nuclear genomes. His laboratory has also shown that mtDNA damage develops in the brains of older mice and in a chemical model of Parkinson's disease. "We have demonstrated that reactive oxygen species cause significantly more mitochondrial DNA damage than nuclear damage in cells from human to yeast, and I am enthusiastic about moving this exciting assay from the bench to the bedside," he said.

Dr. Runge, who is now chair of the Department of Medicine at the University of North Carolina at Chapel Hill School of Medicine, noted the value of a test for mtDNA damage developed for broad clinical application. He commented, "In collaboration with Transgenomic we will be able to pursue studies of large populations of individuals at risk of cardiovascular diseases, and determine the utility of this measure in patients who may benefit from therapies to reduce oxidative stress."

Craig Tuttle, CEO of Transgenomic, commented, "We are pleased to conclude a license with the Clayton Foundation to develop this technology, which it has supported for many years. The license complements Transgenomic's mtDNA mutation analysis capabilities, and demonstrates continued strategic commitment to the rapidly growing area of mitochondrial analysis for pharmacogenomic research and clinical applications."

About Mitochondrial DNA Tests from Transgenomic

Mitochondria are organelles that produce the energy required for cells to function normally. There are hundreds of mitochondria in each cell, and within each mitochondrion are approximately 5 to 10 circular mtDNA molecules. These are maternally inherited, distinct from nuclear DNA, and encode a small number of mitochondrial genes, including elements of the oxidative phosphorylation (OX-PHOS) machinery that manufactures ATP, the biochemical energy currency. That same
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SOURCE Transgenomic
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