NIH Radio
Study Links Faulty DNA Repair to Huntington's Disease Onset
Brief Description:
New insights into how cells repair their DNA could point the way to a possible way to stop or slow the onset of Huntington's disease.
Transcript:
Akinso: New insights into how cells repair their DNA could point the way to a possible way to stop or slow the onset of Huntington's disease according to a study funded by the National Institute of General Medical Sciences, the National Institute of Neurological Disorders and Stroke and the National Institute of Environmental Health Sciences. Huntington's disease is an inherited condition affecting roughly 30,000 Americans. It causes certain nerve cells in the brain to waste away causing such problems as uncontrolled movement, clumsiness or balance problems. Dr. Jeremy Berg, Director of the NIGMS, discusses the importance of this discovery.
Berg: What the paper reports is that a pathway involved in DNA repair seems to be responsible for genetic changes which are seen in Huntington's disease. What's most remarkable about it is it's one particular DNA repair enzyme that seems to be solely responsible which as has both implications for understanding the nature of these genetic changes but also has potential for therapeutic implications longer term.
Akinso: The study shows that the inserted segment grows when cells try to remove oxidative lesions which are caused by byproducts of the oxygen we breathe. DNA enzymes initially keep oxidative lesions in check, but over time, increasing numbers of lesions overwhelm the repair systems. Dr. Berg said while scientists have long suspected that oxidative lesions play a role in Huntington's disease, the specific role of the lesions had remained elusive till now. This is Wally Akinso at the National Institutes of Health Bethesda, Maryland.
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