Researchers at the University of Alabama at Birmingham (UAB) have identified a set of experimental drugs called LRRK2 inhibitors that may go beyond symptom relief to directly counter the inflammation and nerve cell death at the root of Parkinson’s.

These effects have been suggested in mouse and cell culture studies meant to approximate human disease.

Most Parkinson’s disease (PD) patients are still treated with a 42-year-old drug called L-DOPA, which temporarily staves off symptoms but can itself cause heart arrhythmias, stomach bleeding and hallucinations.

This punishing experience may explain in part why patients with PD die at twice the rate of those without the disease in the years after their diagnosis.

“We don’t yet know what percentage of patients might benefit from LRKK2 inhibitors, but LRRK2 is without a doubt the most exciting target for neuroprotection to have ever been identified in Parkinson’s disease,” says Andrew West, Ph.D., associate professor in the Department of Neurology within the UAB School of Medicine.

While West’s compounds are promising, they still face many crucial tests that will decide whether or not they reach human trials. But the field is excited, because this is the first time such a drug target has been found for any neurodegenerative disease.

Along with evidence that LRRK2 plays a crucial role in the mechanisms of Parkinson’s disease, it is a protein kinase, the same kind of enzyme (although not the same one) that has been safely and potently targeted by existing treatments for other diseases, including the cancer drugs Herceptin, Tarceva and Erbitux.

The research also has been funded by private philanthropists within the Birmingham community who are dedicated to advancing new drugs to treat PD. West is the John A. and Ruth R. Jurenko Scholar at UAB, which reflects the Jurenko family’s vital support of this work.