Julie K. Andersen, Ph.D., Professor

Understanding cell death in Parkinson’s disease

Dr. Andersen’s laboratory studies the molecular and cellular bases for Parkinson’s disease (“PD”), an incurable, progressive neurodegenerative disorder which currently affects over 1.5 million people in the U.S. and whose numbers are expected to rise as increasing numbers of individuals in this country live beyond the age of 65. The symptoms of PD include tremor, slowness of movement, rigidity and problems with balance.

Extensive epidemiological data in humans and studies in animal models of PD have long suggested that sporadic forms of the disorder are not strictly genetic in nature but most likely result from combined environmental exposures over the period of the lifespan coupled with increased genetic susceptibilities. Losses in levels of the antioxidant glutathione in susceptible neurons appears to be an early event in the disorder but it is not clear if this is related to the subsequent neurodegeneration.

In an important finding published in the prestigious Journal of Neuroscience in December of 2007, the Andersen laboratory demonstrated that inducing glutathione loss results in an age-related neuronal cell loss akin to that which occurs in human PD. This provides an important new animal model for testing the efficacy in glutathione replacement as a treatment for the disease.

In a second publication in the journal PLos One, the laboratory showed that increasing levels of the enzyme monoamine oxidase B (MAO-B), which is known to increase with age in the brain and whose inhibition is targeted by the drug selegiline, also results in PD-like neurodegeneration. This suggests that MAO-B increase can predispose individuals for the disorder and that early treatment with inhibitors may be warranted in those persons with higher genetic levels.