The study, led by Buck faculty member Julie Andersen, PhD, has suggested that preventive treatment may be useful for those who have high levels of MAO-B, an enzyme that regulates nerve activity in the brain and leads to Parkinson's-like symptoms in mice genetically engineered to overexpress the protein.

Also, the drugs in use these days as and additional therapy for PD in humans prevented the development of its symptoms in these same animals. Also, drugs currently used as an adjunct therapy for Parkinson's in humans.

It is well known that measurable levels of MAO-B vary 50-fold in humans and tend to increase with age. It has also been suggested through many studies that increases in MAO-B leads to neurodegeneration associated with PD, but direct proof of a causative role for the enzyme has not yet been found.

Since a long time, a drug called deprenyl, which inhibits MAO-B, has been used as a therapy for Parkinson's in combination with other drugs that boost the level of dopamine, an important neurotransmitter that is preferentially reduced in the disease.

According to clinical studies, the fact that deprenyl treatment solely does not have any impact on mortality associated with Parkinson's, has raised doubts on the role of MAO-B in the disease itself. However, Andersen claimed that this might not be true.