Originally published October 12 2005
Mayo Clinic makes discovery about DNA repair
by Mike Adams, the Health Ranger, NaturalNews Editor
The discovery made by Mayo Clinic researchers about why certain DNA repair processes may fail could lead to an eventual discovery of how to avoid Huntington's disease.
The Mayo team discovered that under certain conditions, a key protein fails to recognize a specific form of DNA that it needs to begin the repair process by recruiting additional proteins.
They report their findings in a recent issue of Nature Structural and Molecular Biology.
(http://www.nature.com/nsmb/journal/v12/n8/pdf/nsmb965.pdf). By failing to initiate repair, the defective mechanism may give rise to disabling inherited brain diseases such as Huntington's disease, which causes select brain nerve cells to waste away. Huntington's affects 30,000 adults in the United States, and another 150,000 Americans may be at risk of inheriting it. Friedreich's ataxia is another neurodegenerative disease that may one day have a treatment based in part on this finding, as could a form of heritable colon cancer (hereditary non-polyposis colon cancer).
"Hereditary neurodegenerative diseases such as Huntington's disease have no cure and no effective therapy," says Cynthia McMurray, Ph.D., Mayo Clinic molecular biologist and lead investigator of the study.
"Since the mutation initiates coding for the defective, toxic protein, we feel that it is likely that a successful effort to stop the steps leading to mutation will likely stop the progression of disease."
A commentary accompanying the journal article (http://www.nature.com/nsmb/journal/v12/n8/pdf/nsmb0805-635.pdf) welcomes the clarity the Mayo work brings to the problem of DNA's abnormal expansion within a cell, which appears to be the underlying condition that leads to the repair defect.
From bacteria to humans, cells have evolved sophisticated means of repairing DNA that gets damaged -- by a variety of causes -- ranging from environmental stresses to inherent copying errors.
Dr. McMurray's group studied a specific mismatch repair protein Msh2-Msh3 and found a paradox: Instead of helping repair DNA damage, under certain conditions, Msh2-Msh3 was actually harming the cell.
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