Growth Factor Promotes New Neuron Growth in Mouse Model of Parkinson's Disease

Newswise — Mice induced to develop Parkinson’s disease (PD) show an increase in the growth of new neurons after they are treated with a well known growth factor. The research, to be published May 16 in The Journal of Neuroscience, based on work by scientists at the Buck Institute, highlights a potential new therapy for this incurable, neurodegenerative disorder that affects 1.5 million Americans.

The mice, which developed Parkinson-like symptoms after they received the toxin MPTP (which causes PD in humans) were treated with fibroblast growth factor-2 (FGF-2), a naturally occurring protein that has been studied extensively for its neuroprotective properties. In the Buck study, the use of FGF-2 enhanced the neurogenesis, or growth of new neurons, that was already underway in the injured area of the brain. In addition, researchers began to see an increase in the cells that produce dopamine, the neurotransmitter implicated in PD.

“The fact that FGF-2 allowed these new neurons to develop in the principle site of cell loss in the disease is quite exciting,” said Buck faculty member and lead scientist Julie Andersen, PhD. “This suggests that administration of growth factors might be used therapeutically to replace dead or damaged cells. The next step in our research is to see whether treatment with FGF-2 results in any symptomatic improvement in the mice.”

Scientists at the Buck are currently researching FGF-2 as a potential treatment for Huntington’s disease, a fatal hereditary brain disorder that affects approximately 30,000 Americans. In partnership with Neurobiological Technologies, Inc. (NASDAQ: NTII), Buck researchers are seeking to create a form of FGF-2 for human clinical trials. The protein shows particular promise because it is able to cross the blood-brain barrier.

This most recent study highlights the interdisciplinary approach to research at the Buck Institute. This work built on earlier discoveries in the laboratory of David Greenberg, MD, PhD, which showed neurogenesis occurring in the brains of patients diagnosed with Alzheimer’s disease, and the laboratory of Lisa Ellerby, PhD, which showed that FGF-2 promoted new nerve growth and increased survival in mice genetically engineered to develop Huntington’s disease. The work as a whole emphasizes a research focus at the Buck Institute on efforts to enhance the brains ability to heal itself in the face of injury.

Joining Andersen in the study were Jun Peng, Lin Xie, Kunlin Jin, and David A. Greenberg, all of the Buck Institute.

The Buck Institute is an independent non-profit organization dedicated to extending the healthspan, the healthy years of each individual’s life. The National Institute of Aging designated the Buck a Nathan Shock Center of Excellence in the Biology of Aging, one of just five centers in the country. Buck Institute scientists work in an innovative, interdisciplinary setting to understand the mechanisms of aging and to discover new ways of detecting, preventing and treating age-related diseases such as Alzheimer’s and Parkinson’s disease, cancer, stroke, and arthritis. Collaborative research at the Institute is supported by genomics, proteomics and bioinformatics technology. For more information: www.buckinstitute.org.