2016 RLS Research Grants were awarded to:
William Padula, PhD, MS, MSc
The first in 2016, a $36,750 grant was awarded to William Padula, PhD, MS, MSc, of the Johns Hopkins Bloomberg School of Public Health, for a research study to assess the economic burden of RLS over the lifetime of the disease. This study will evaluate the direct and indirect costs of RLS diagnosis and treatment, as well as costs related to loss of work and time by individuals living with RLS. Findings will potentially help increase future RLS research funding from agencies such as the National Institutes of Health (NIH).
2015 RLS Research Grants were awarded to:
Yuqing Li, PhD
Dr. Li will continue his research on the role of the MEIS1 gene in RLS. In this study, called “Characterization of MEIS1 heterozygous knockout mice as a model of Willis-Ekbom disease,” the researchers will perform a detailed analysis of MEIS1 mutant mice. They will look at whether the MEIS1 mutant mice show other RLS symptoms such as changes in sensation.
They will also examine the brain’s dopamine system and determine what areas are affected by the MEIS1 mutation. Dr. Li's group will try to treat a group of MEIS1 mutant mice with known dopamine drugs used in RLS patients to see whether these drugs alleviate the RLS symptoms in these mice. The goal is to validate the MEIS1 mutant mice as a useful model for testing other potential treatments for RLS.
Sergi Ferré, MD, PhD
Dr. Ferrés research will explore cortico-striatal transmission in iron-deficient rats as a model for screening of drugs potentially useful in treatment of restless legs syndrome.
There are multiple potential medications that for theoretical reasons should be considered beneficial for RLS, but many of these are not available for human use and, for those that are available, testing them in RLS patients would be expensive and time consuming. Efficient drug screening is needed to select drugs that seem promising for RLS, which could then be studied in RLS patients. This project aims at obtaining a new animal model for such screening.
The first goal of the project is to demonstrate that iron deficiency in rats is associated with increased cortico-striatal glutamatergic transmission. The second goal will be validating our model by demonstrating the ability of drugs already known to be efficient in RLS patients to revert the changes induced by iron deficiency on cortico-striatal neurotransmission in rats. The model would then be used to screen new compounds that could potentially be potent modulators of cortico-striatal neurotransmission.