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We are pleased to announce our fourth annual Dravet Syndrome Research Award focused on exploring therapeutic approaches and causative factors for Dravet Spectrum Disorders, including Dravet syndrome and related pediatric epilepsy disorders will be awarded in 2013.
Details about the award, including the amount, will be announced here in April, 2013.
Established and new investigators may apply for this award. Applications will be judged according to relevance, quality of research lab, scientific merit, and potential for new therapeutic approach as determined by Dravet.org's Scientific Research Review Committee, a distinguished group of research scientists.
For application, guidelines and inquiries, contact Joan Skluzacek, at info@dravet.org or 866-828-1843.
The 2011 Research Award was given to Dr. Beverly Wical at Gillette Children’s Specialty Healthcare in St. Paul, Minnesota.
This two-year $30,000 award was funded in honor of DEREK RUDAWSKY through the loving efforts of his parents, family and friends who organize and participate in the annual DEREK’S DASH.
Dr. Wical’s study, Verapamil as Adjunctive Seizure Therapy for Children with Dravet syndrome, seeks to assess the efficacy of verapamil as an adjunctive therapy for improving seizure control (generalized tonic-clonic, secondarily generalized tonic-clonic, and clonic or hemiclonic) and to assess signs of dysautonomia before and after treatment. Verapamil, a calcium channel blocking agent, may play a role altering autonomic tone abnormalities in children with Dravet syndrome and may be a part of the mechanism that leads to improved seizure control. This will serve as a pilot study for gathering data in hopes of extending and expanding positive results with the goal of leading to a larger, controlled trial.
The 2010 Research Award was given to Dr. Jing-Qyong Kang of Vanderbilt University Medical Center in Nashville, Tennessee.
Dr. Kang’s study, Toward understanding the GABRG2 truncation mutations associated with epilepsy and Dravet syndrome, seeks to understand 1) why the truncation mutations in GABAA receptor g2 subunit cause epilepsies and 2) why some mutations cause mild febrile seizures, while the others cause more severe epilepsy, like Dravet syndrome. The characterization of the altered signaling pathways of these misrouted and misfolded GABAA receptors which result from truncation mutations may help to 1) understand why Dravet syndrome is different than other mild epilepsies caused by the same gene mutations? 2) elucidate the "vaccine damage" in those children with Dravet syndrome who had an encephalopathy with refractory seizures and intellectual impairment after vaccination; 3) solve the long time enigma of the relationship between hippocampal atrophy and epilepsy ("which comes first, the chicken or the egg?"); 3) identify a potential novel therapy for treating Dravet syndrome.
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