A key enzyme plays an important role in the development of Parkinson's disease

Researchers from Johns Hopkins say they found two important new clues in the process of battling with Parkinson's disease: blocking an enzyme called c-Abl can protect specially-bred mice from suffering the disease, while the chemical marker of the second protein may indicate the presence of the disease and its severity. Their work not only provides a promising target for the drug development but also provides tools to more broadly accelerate Parkinson's disease research. The research results were published online on June 27 in the Journal of Clinical Research. This journal also published some other studies on recombinant mouse proteins and recombinant horse proteins.

Parkinson's disease is a progressive neurological disease which affects movement. Autopsies showed the c-Abl was very active in the brain of patients with the disease. In addition, in the study of specially-bred mice which were prone to the disease, the researchers found that the drugs which blocked the c-Abl may play a role in preventing or delaying the disease. However, assistant professor of neurology Dr Han Seok Ko at John Hopkins said, "Those drugs used in the study may also block other similar proteins, so we're not sure blocking c-Abl is the reason that prevent animals from showing symptoms or affect the disease progression."

The researchers' new experiment began from the condition that the mice were genetically modified so that they got the disease. If "knocking out" the gene carrying c-Abl, the symptoms of the disease will be reduced. Conversely, if changing the genes and increasing levels of c-Abl, the symptoms of the disease in mice will increase and the deterioration will accelerate. The researchers said the increase in the number of c-Abl also make normal mice suffering from Parkinson's disease.

To understand more about the mechanisms of disease, the researchers inspected the interaction between c-Abl protein and another protein α- synuclein. We all knew that α- synuclein clump in brain is a hallmark of Parkinson's disease. Researchers from Johns Hopkins found that the c-Abl adds a molecule called phosphate group to a specific site on the α- synuclein, while the continuous increase of c-Abl levels will lead to more α- synuclein aggregation and worsening of symptoms.

"We plan to study whether α- synuclein protein carrying a phosphate group at the site where c-Abl targeted on can be used to measure the severity of Parkinson's disease. There is no such biochemical measurements exist, and it hinders research on potential therapies of the disease," Dawson represented. More research would be done using recombinant Cdh2.