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Grant recipients were selected with the invaluable assistance of the CURE Scientific Advisory Board and the CURE Research Review Board.

2013  |  2012  |  2011  |  2010  |  2009  |  2008  |  Older

CURE grant award Grants marked with an asterisk are made possible by individuals, families, foundations, or corporations.

2010 Research Awards

Challenge Awards
Two- to three-year grants for established investigators

CURE grant award The Brighter Future Award
In honor of Lauren Axelrod, funded by a caring donor
Yellen / Danial

Gary Yellen, PhD and Nika Danial, PhD
Harvard Medical School; Dana-Farber Cancer Institute

“Seizure Resistance through Metabolic Control in Novel Mouse Model”

Nearly one-third of people with epilepsy have seizures that cannot be well-treated by existing medications. The success of dietary treatment (such as the ketogenic diet) for many of these individuals suggests a powerful connection between metabolism and seizures. However, these diets are difficult to maintain, spurring a search for alternative ways to manipulate metabolism in order to prevent seizures. Drs. Danial and Yellen are collaborating on a multi-disciplinary approach to this problem based on an exciting initial observation. They found that a genetic manipulation in mice that reduces the metabolism of glucose (sugars) and enhances the metabolism of ketone bodies (compounds which are a vital source of energy in the brain during fasting) can produce strong seizure resistance, which is far more dramatic than seen with the ketogenic diet. They will explore the mechanism of this effect and investigate novel therapeutic targets and approaches for epilepsy treatment.



CURE grant award The 2010 Falk Medical Research Trust Award
Roper

Steven Roper, MD
University of Florida

“Treating Cortical Dysplasia with Adult Human Neural Progenitor Cells”

Cortical dysplasia (CD) is a problem of brain development that often causes severe epilepsy. Using an animal model of CD, Dr. Roper and his collaborators will use a novel approach to the treatment of epilepsy in CD using adult human neural progenitor cells from surgically removed tissue from individuals with intractable epilepsy. These cells will be put into rats with CD in order to replace the lost inhibitory neurons and restore normal brain function. This project offers a new direction for treatment of intractable epilepsies using targeted cellular therapies. If this research is successful, the use of adult human donor cells will facilitate the translation of this approach to treatments for individuals with epilepsy due to CD.



Prevention of Epilepsy After Brain Injury Award
Two- to three-year grants in support of research preventing or treating post-traumatic epilepsy

CURE grant award The Friends for a Cure Award
This grant was funded by donations
made for CURE’s fall 2009 Every Dollar Counts campaign.
Mody

Istvan Mody, PhD
UCLA School of Medicine

“Prevention of post-stroke epileptogenesis”

Cerebrovascular brain injuries (including stroke and ischemia) account for 11% of the symptomatic epilepsies and the incidence of epilepsy after a stroke can be as high as 20%. Dr. Mody has developed a novel and specific cerebrovascular trauma model in mice that reduces the blood supply to brain areas heavily involved in the genesis of epilepsy, and has preliminary data consistent with the development of epilepsy after such trauma. His investigation will focus on understanding the mechanisms leading to the development of epilepsy after the cerebrovascular injury, and on developing novel pharmacological approaches aimed at stopping the transition from stroke to epilepsy in its tracks.



Multidisciplinary Award
Two- year grants in support of collaborative research

CURE grant award The Heldman Award
Kayak / Russek

Amy Brooks-Kayal, MD and Shelley Russek, PhD
University of Colorado Denver/The Children's Hospital; Boston University School of Medicine

“JaK/STAT inhibition to prevent epilepsy development and progression”

Drs. Brooks-Kayal and Russek will examine the role of an important cell signaling pathway called the Jak/Stat pathway in the development and progression of epilepsy. Their labs recently discovered that this pathway regulates brain inhibition and is activated by seizures, likely in response to an increase during seizures of the growth factor, brain derived neurotrophic factor (BDNF). Using a combination of studies in the laboratory and in animal models of epilepsy, they will use specific blockers of BDNF and the Jak/STAT pathway to reduce or prevent epilepsy development and/or progression.



SUDEP Awards
One-year grants in support of SUDEP research

CURE grant award Dravet Syndrome Foundation & CURE Award
Maier / Mantegazza

Sebastian Maier, MD, PhD and Massimo Mantegazza, PhD
University Hospital of Wuerzburg; IPMC, Nice-Sophia Antipolis, France

“Cardiac arrhythmias and SUDEP in SMEI and other Nav1.1 (SCN1A) related epilepsies”

Dravet syndrome is a severe and drug resistant form of epilepsy, characterized by high mortality rates. Sudden unexpected death in epilepsy (SUDEP) is the most frequent cause of death for individuals with Dravet syndrome. The majority of individuals with Dravet syndrome carry mutations in a sodium channel subtype that is found in the brain, heart and nerves. Drs. Maier and Mantegazza will study the role of this sodium channel subtype in the heart in a model of Dravet syndrome in order to investigate the occurrence and mechanism of arrhythmias and their possible involvement in SUDEP.



CURE grant award The Leisher Family Award
Tomson / Mattsson

Torbjorn Tomson, MD, PhD and Peter Mattsson, MD, PhD
Karolinska Institutet; Uppsala University

“Role of pharmacological treatment in the prevention of SUDEP”

Drs. Tomson and Mattson will utilize three nation-wide Swedish registries that offer unique opportunities to study the association between drug treatment and risk of sudden unexplained death in epilepsy (SUDEP). The medical records of living individuals with epilepsy will be compared to those with SUDEP with respect to use of antiepileptic drugs (AEDs) and other drugs to assess if the risk of SUDEP is related to non-adherence to prescribed AEDs, to any specific type of AED, and if concomitant use of other drugs such as some antidepressants could be protective. This study will provide essential information for the development of pharmacological treatment strategies to reduce the risks of and to prevent SUDEP.



CURE grant award The 2010 Christopher Donalty & Kyle Coggins Memorial Award
for SUDEP Research
Faingold

Carl Faingold, PhD
Southern Illinois University School of Medicine

“Prevention of SUDEP by Serotonergic Agents in DBA/1 Mice”

Dr. Faingold has developed a new animal model of human sudden unexpected death in epilepsy (SUDEP), DBA/1 mice. These animals show generalized seizures and then stop breathing if not resuscitated, which is common in human SUDEP. They found that drugs that increase the level of a neurochemical (serotonin) in the brain will prevent SUDEP in these mice. The current study will examine if new drugs that have a more selective effect on serotonin will prevent the respiratory arrest that follows seizures in these mice.



Innovator Awards
One-year grants in support of the exploration of a highly innovative new concept or untested theory that addresses an important problem relevant to epilepsy

Carmant

Lionel Carmant, MD
University of Montreal

“A New Experimental Model of Rasmussen's Encephalopathy: Understanding its Pathophysiology”

Rasmussen encephalitis (RE) is a rare but severe brain disorder that starts in childhood with seizures that become more and more frequent, as well as a progressive weakness of the affected side. The mechanisms of RE are still not well understood, even if some experimental data suggest an immune mediated disorder. By injecting RE patients’ blood cells into severely immunologically-compromised mice, we are able to induce seizures and produce pathological findings in the mouse brain similar to pathological lesions observed in children with RE. We can also use frozen blood cells from individuals with RE, making our strategy to understand the pathophysiology of RE even more feasible. Preliminary data shows that RE is mediated by the immune system, and that seizures are due to the release of inflammation products followed by an infiltration of white blood cells in the brain. The model we will use for this research will allow us to identify the cells responsible for RE and to precisely determine the role of the immune system in this rare disorder. In the future, we plan to utilize this model test to new therapeutic strategies for RE.



Patel

Manisha Patel, PhD
University of Colorado, Denver

“Treatment of Epilepsy with a Catalytic Antioxidant”

The vast majority of epilepsy research is focused on channels and synapses and only a minority focuses on metabolic processes. Although anticonvulsant drugs remain frontline therapies for controlling epilepsies, the search for novel disease-modifying drugs is highly desirable to halt the devastating effects of chronic seizures. Catalytic antioxidants are small molecule mimics of the body’s own defenses that can efficiently remove reactive oxygen species and in the process, regenerate themselves. The goal of this project is to conduct a proof-of-principle study to determine if early treatment with a novel catalytic antioxidant prevents metabolic dysfunction and epilepsy in mice lacking a critical mitochondrial antioxidant.



Rotenberg

Alexander Rotenberg, MD, PhD
Children’s Hospital Boston/Harvard Medical School

“Prevention of Post-Traumatic Epilepsy by Application of Ceftriaxone Acutely After TBI”

Traumatic brain injury (TBI) often leads to epilepsy with a delay that can be weeks to months after the initial trauma. At the biochemical level, the process that leads to epilepsy after TBI is in part mediated by an excess of the excitatory neurotransmitter glutamate whose concentration rises sharply after injury. Ceftriaxone and similar antibiotics, independent of their antibacterial properties, can increase function and expression of the glutamate transport protein, GLT1, which may remove excess glutamate after injury. Accordingly, we propose to test a novel application of ceftriaxone, acutely after brain injury when the biochemical changes leading to post-traumatic epilepsy are first emerging. Specifically we propose to use the established rat lateral fluid percussion injury (LFPI) severe TBI model in a preclinical trial to test whether daily injection of ceftriaxone acutely after TBI can (1) enhance GLT1 function and limit glutamate accumulation after injury, (2) limit cell death and (3) reduce the likelihood of seizures after TBI. As ceftriaxone and similar compounds are already in wide use for antibacterial treatment, we anticipate that positive data from the proposed experiments can be rapidly translated to novel clinical trials.

 

See previous years' CURE grant recipients:
2013  |  2012  |  2011  |  2010  |  2009  |  2008  |  Older

 

CURE For questions, please contact Julie Milder at the CURE office, 312.255.1801, or email julie@cureepilepsy.org.

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