Hereditary neurodegenerative diseases such as Huntington's disease have no cure and no effective therapy. 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.

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Towards this goal, we are currently dissecting the molecular mechanism by which the aborted function of this repair enzyme attenuates its normal repair pathway. This is crucial information for understanding how to design new drugs or other interventions that help patients.

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