Julie K. Andersen, PhD
Dr. Andersen is a Professor at the Buck Institute for Age Research in Novato, California. Her research focuses on the role that oxidative stress plays in neurodegeneration both during normal aging and as a cause of certain neurodegenerative disease states. Dr. 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.
As a Brookdale National Fellow, Dr. Andersen's work involved the creation of transgenic mouse models with altered expression of either antioxidant enzymes or iron-binding proteins that may act to alter the organism's response to free-radical damage resulting in changes in neuronal degeneration. It has been postulated that iron-induced oxidative stress and/or decreased levels of certain free-radical scavenging enzymes in the brain may play a major role in neurodegenerative diseases including Parkinson's as well as in the degeneration of neurons seen during the normal aging process. The animals produced from these studies will act as a model for identifying those individuals with genetic predispositions for increased free radical production who would be likely to benefit from preventative antioxidant therapy. This work resulted in a publication in the prestigious journals Neuron in 2003, the Journal of Neuroscience in 2007, and PLos One in 2008. Dr. Andersen completed her PhD in Molecular Neurobiology at the UCLA School of Medicine in Los Angeles in 1989 and received her post-doctoral training in Neuromolecular Genetics at the Massachusetts General Hospital in Boston. She joined the Gerontology faculty at the University of Southern California in September of 1993 then transferred to the Buck in the fall of 2000.
Internationally renowned for her work on Parkinson's disease, Andersen's continuing work includes examining the mechanisms underlying iron dysregulation and oxidative stress that impact on susceptibility to Parkinson's disease. 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 diseas, and also the identification of novel mechanisms involved in mitochondrial dysfunction associated with Parkinson's including alterations in glutathione and monoamine oxidase B levels.
Brookdale Fellow Class of 1994