Buck research focuses on risk factor for Parkinson's disease

A new study demonstrates that high levels of MAO-B, an enzyme that regulates nerve activity in the brain, cause Parkinson’s-like symptoms in mice genetically engineered to overexpress the protein. Furthermore, drugs currently used as an adjunct therapy for Parkinson’s in humans prevented the development of Parkinson’s symptoms in these same animals. The findings, by scientists at the Buck Institute for Age Research, raise the possibility that humans could be tested to see if they have a risk factor for the progressive, incurable neurodegenerative disorder that affects 1.5 million Americans and receive preventive treatment. The study appears in the February 20 issue of the open-access, online journal, PLoS ONE.