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Dr. Julie Andersen studies the molecular and cellular mechanisms that give rise to Parkinson’s disease. Andersen, among others, has shown that the neuronal death associated with Parkinson’s may be caused by an increase in oxidative stress within nerve cells, and that the development of Parkinson’s could involve environmental factors as well as genetic predisposition to the disease.

Internationally renowned for her work on Parkinson’s disease, Andersen continuing work includes examining the regulation of iron levels in newborns and their subsequent susceptibility to Parkinson’s, environmental exposure to the herbicide paraquat as a risk factor for Parkinsonian neurodegeneration, the effects of decreases in antioxidant levels (specifically glutathione) associated with the onset of Parkinson’s, and the consequences of the age-related increase in an enzyme involved in dopamine metabolism (monoamine oxidase B). All of the projects studied in the Andersen lab provide critical information about potential therapeutic targets, some of which are already being tested, including the use of drugs to redress iron imbalances, and others to decrease oxidative stress.

Some of Andersen’s key findings include demonstrating that iron is actively involved in neurodegeneration and is not just a by-product of Parkinson’s disease, and also the identification of novel mechanisms involved in mitochondrial dysfunction associated with Parkinson’s including alterations in glutathione and monoamine oxidase B levels.