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Excess DNA damage found in cells of patients with Friedreich's ataxia
Date:1/14/2010

severely affected. Patients typically require wheelchairs within 10 to 20 years after symptoms begin.

For the study, the researchers profiled gene activity in blood samples from FRDA children to search for biomarkers of the disease, as compared to young healthy donors. Those data were compared to blood tests from FRDA adults, and the latter compared to a second group of healthy individuals.

"We saw gene activity patterns that are associated with responses to DNA damage, and our comparisons and follow-up tests showed us that FRDA patients have far more damage than seen in healthy people," said Dr. Van Houten, who noted that everyone has some DNA damage, at various stages of repair, in their cells. "We found gene expression signatures that correlated with frataxin levels, age of disease onset and a standardized measure of patient disability."

"If further testing validates the set of genes and activity profiles as predictive biomarkers, they could be useful in assessing the current status of a patient's illness as well as the response to experimental therapies in clinical trials," he said. "Also, new drug targets might be found in the DNA repair and iron-processing pathways affected by the lack of frataxin, generating much-needed treatment breakthroughs."


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Contact: Anita Srikameswaran
SrikamAV@upmc.edu
412-578-9193
University of Pittsburgh Schools of the Health Sciences
Source:Eurekalert

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