With this award Dr. LoGrasso joins the LKRR2 Consortium, established last year by the Michael J. Fox Foundation. The consortium is an international group of academic and industry partners dedicated to accelerating LRRK2 therapeutic development.
"I want to thank the Fox Foundation for their generous grant," LoGrasso said, "and for giving me the opportunity to study the links between these intriguing genetic mutations. The question our laboratory will explore is how SGK1 works and how it impacts the LRRK2 mutation. We're all hoping that ultimately this produces a new target for treatment intervention because there are no viable long-term treatments available today."
Since the 1960s the mainstay for the treatment of Parkinson's disease has been levodopa (L-DOPA), a drug that provides only symptomatic relief. Unfortunately, L-DOPA loses efficacy over time and has numerous side effects that limit its effectiveness.
Patients with Parkinson's disease suffer from a loss of dopaminergic neurons in a specific area of the brain. An estimated one million Americans are believed to suffer from the disease, according to the Parkinson's Disease Foundation; approximately 40,000 new cases are reported annually.
The LRRK2 gene was first linked to Parkinson's disease in 2004, and many believe it to be the most common genetic contributing factor to the disease. While hereditary forms of the disease are relatively rare an estimated five to 10 percent unlocking the mechanisms involved in both LRRK2 and SGK1 could eventually benefit all patients.
Mutations in the LRRK2 gene have been linked with an increased risk not only of Parkinson's disease, but also of Crohn's disease. SGK1 is involved in a number of biomolecular processes including inflammation, cell proliferation, and apoptosis or programmed cell death. It is believed that the gene also plays a role in brain disorders other than Parkinson's disease, such as schizophrenia
|Contact: Mika Ono|
Scripps Research Institute