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

CURE grant recipients by year:
2016  |  2015  |  2014  |  2013  |  2012  |  2011  |  2010  |  2009  |  2008  |  Older

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

* The 2008 Falk Medical Research Trust Award *
Michael Wong

Michael Wong, MD, PhD
Washington University, St. Louis, MO

“Stabilizing Dendritic Structure as a Novel Treatment for Epilepsy”

Injury to the brain caused by repeated seizures may contribute to cognitive dysfunction and other neurological deficits in epilepsy patients. In this three-year project, Dr. Wong will investigate the direct effects of seizures on dendrites and dendritic spines, which are key components of synapses and potential sites of learning and memory in the brain. He will utilize modern cellular imaging techniques to visualize structural changes in dendrites in mice before and after seizures. The molecular mechanisms underlying these changes during seizures will be explored. Finally, drugs that can inhibit this dendritic injury will be tested, potentially leading to novel treatments for preventing seizure-induced brain injury.

* The 2008 Northwestern Dance Marathon Award *
Steven Bealer

Steven L. Bealer, PhD
University of Utah, Salt Lake City, UT

“Predictors of Cardiac Risk and Beneficial Effects of Pharmacotherapy in Epilepsy”

In patients with epilepsy, sudden cardiac death may occur following status epilepticus (prolonged seizures), in sudden unexplained death in epilepsy (SUDEP), and in patients with epilepsy and co-existing cardiac disease. However, the relationship between epilepsy, clinical indicators of cardiac risk, and the beneficial effects of drugs that protect the heart are not known. In this three-year project, Dr. Bealer will evaluate these relationships to determine which patients should be routinely evaluated for cardiac risk, and whether appropriate cardiac drug therapy reduces the risk of death.


Multidisciplinary Awards
One-year grants in support of collaborative research

* The 2008 Christopher Donalty and Kyle Coggins Memorial Award
for Multidisciplinary Research *

Dmytro Isaev, PhD
Bogomoletz Institute of Physiology, Kiev, Ukraine

Gregory L. Holmes, MD
Dartmouth Medical School, Lebanon, NH

“Reduction in Seizure Susceptibility through Modification of the Level of Extracellular Sialic Acid”

Far too many individuals with epilepsy who take antiepileptic drugs continue to have seizures or suffer from serious medication side effects. Working together, Dr. Holmes (a pediatric neurologist) and Dr. Isaev (a senior researcher in general physiology of the nervous system) recently showed that they could dramatically reduce seizures by altering a naturally occurring compound in the brain called sialic acid. By reducing sialic acid, they have been able to turn down “the thermostat of the brain,” reducing brain excitability without causing any substantial side effects. In this one-year study, Drs. Holmes and Isaev will build upon these exciting preliminary results and determine whether modification of sialic acid reduces seizures in a mouse model of epilepsy and prevents the onset of epilepsy following brain injury.


Gregory Mathews, MD, PhD
Vanderbilt University Medical Center, Nashville, TN

David Poulsen, PhD
University of Montana, Missoula, MT

“Targeted Enhancement of GABA Synthesis for Epilepsy Therapy”

Despite a dramatic increase in new drugs available for epilepsy patients, more than 30% of patients still do not achieve seizure freedom. Therapies aimed at increasing GABA, the major neurotransmitter in the brain, are key targets for anticonvulsant therapies. However, traditional medications are heavily sedating with significant cognitive side effects. This one-year collaborative effort between Dr. Poulsen (a molecular virologist) and Dr. Mathews (a clinical epileptologist and basic neuroscientist) will explore the use of viral gene technology for enhancing GABA, offering the promise of new and less debilitating therapeutic options for epilepsy patients.


Quest Awards
One-year grants for both established and early career investigators

* The 2008 UCB Diamond Sponsorship Award *
Christophe Bernard

Christophe Bernard, PhD
INSERM, Marseille, France

“Dendritic HCN Channels as a Target against Epileptogenesis and for Improving Cognitive Deficits in Temporal Lobe Epilepsy”

In addition to seizures, many patients with epilepsy struggle with memory and other cognitive deficits. Dr. Bernard has shown that temporal lobe epilepsy is associated with a loss of function of a specific protein in the brain called hyperpolarizing-activated cyclic nucleotide-gated ion channels (HCN). This loss not only makes the cell more excitable but also impairs cognitive function. In this study, Dr. Bernard’s goal is to determine whether the loss of HCN may actually cause epilepsy and/or cognitive dysfunction. By boosting HCN activity in animal models of epilepsy, using specific drugs or via genetic technology, this study may lead to new approaches to controlling seizures with the potential of also restoring cognitive function.

* The CURE 365 and Maggie Loeffel Award *
Karin Borges

Karin Borges, PhD
Texas Tech University Health Sciences Center, Amarillo, TX

“Anaplerosis: A Potential New Dietary Therapy for Epilepsy”

Many patients with epilepsy do not respond to drugs or to the high-fat ketogenic diet. Triheptanoin, a tasteless and well-tolerated oil, is a component of the anaplerotic diet. This oil is believed to provide more energy to the brain, which may help to stabilize nerve cell activity and prevent seizures. In this one-year study, Dr. Borges will test, in mice, whether an anaplerotic diet can inhibit seizures. If so, this study could lay the groundwork for future investigation of this novel approach to treating epilepsy.


Traumatic Brain Injury Awards
A Partnership with the United States Army Medical Research and Materiel Command (USAMRMC)


David Prince, MD

Kevin Graber, MD, co-investigator - Stanford University, Stanford, CA

Prevention of Neocortical Post-traumatic Epileptogenesis

There is often a delay between brain injury and development of seizures in lab animals and in humans. Dr. David Prince has shown that development of post-traumatic epilepsy in animals can be prevented by briefly treating the injured brain with a substance that blocks nerve cell messages. In this two-year study, they will use other approaches, such as the application of a drug that acts to decrease the action of an excitatory messenger normally pr esent. Other experiments will test whether increases in a gene that prevents both nerve injury and development of new connections will prevent post-traumatic epilepsy in animals. This grant is jointly sponsored by the USAMRMC and funds raised from the Northwestern University 2007 Dance Marathon.


Detlev Boison, PhD

Theresa Lusardi, PhD, co-investigator - RS Dow Neurobiology Lab, Legacy Research Portland, OR

Prevention of Posttraumatic Epilepsy by Transient Modulation of Adenosine Receptors

Adenosine is one of the brain’s own seizure-control substances and recent evidence suggests that epilepsy development is associated with a failure in the adenosine system. A frequent cause for the development of epilepsy is a previous traumatic brain injury. In this two-year study, Dr. Boison will examine how failures in the adenosine system develop as a consequence of brain injury, how these failures contribute to the development of spontaneous recurrent seizures, and how the development of epilepsy can be prevented by transient application of adenosine-related drugs during a critical window of time after the injury.


Daniela Kaufer, PhD
University of California, Berkeley, CA

Alon Friedman, MD, PhD, co-investigator
Ben-Gurion University of the Negev, Israel

The Role of Serum Albumin and TGF-Beta in Post-Traumatic Epileptogenesis

The mechanism by which traumatic brain injury leads to epilepsy is mostly unknown and, at present, no preventive treatment exists. Dr. Kaufer, along with co-investigator Dr. Alon Friedman of Ben-Gurion University of the Negev Beer-Sheva in Israel, discovered a novel mechanism that occurs following the injury-induced breakdown of the blood-brain barrier, leading to the development of epilepsy. This process is dependent on specific uptake of the serum protein albumin into the "supporting" cells of the brain, known as astrocytes. This two-year project aims to develop therapies that will prevent the generation of epilepsy following brain trauma.


Jian Kang, MD, PhD - New York Medical College, New York, NY

Roles of Glutamate-Induced Astrocytic Glutamate Release in Post-Traumatic Epilepsy

Post-traumatic epilepsy is a common neurological disorder following brain injury. The cellular and molecular mechanism of this disease is still unknown. The goal of this two-year project is to study how glutamate release from astrocytes, the “supporting” cells of the brain, causes the development of post-traumatic epilepsy. In response to increased extracellular glutamate, astrocytes release a large amount of glutamate through fusion of a large vesicle. This may contribute to the cellular mechanism of post-traumatic epilepsy. This work may lead to a novel target for preventing post-traumatic epilepsy following brain injury.


Adi Mizrahi, PhD - The Hebrew University of Jerusalem, Israel

In Vivo Time-Lapse Imaging of an Epileptogenic Focus in Post-Traumatic Epilepsy

In this three-year project, Dr. Mizrahi will study the changes within the brain that underlie the development of post-traumatic epilepsy in mice. He will use live imaging techniques in a mouse model of post-traumatic epilepsy to learn how brain cells react when post-traumatic epilepsy develops. These experiments will provide a direct view, at high resolution, of the actual dynamics of the development of epilepsy. Such in vivo experiments may lead to the discovery of new biological mechanisms that lead to epilepsy after brain injury.


Philip Schwartzkroin, PhD - University of California, Davis, CA

Dietary and Activity Treatments for Modulating Post-Traumatic Brain Hyperexcitability

In this two-year project, Dr. Schwartzkroin will study potential protective therapies in a rat model of traumatic brain injury. He will examine the effects of a ketogenic diet administered both before and after the brain insult, including the potential addictive effects of the diet. In addition, because “enriched environment therapies” have been shown to promote the birth of new brain cells, Dr. Schwartzkroin will study the effects of exposure to such environments. If these simple and inexpensive treatments can reduce the expected brain cell damage associated with traumatic brain injury, and/or prevent the development of abnormal brain excitability, then these therapies could be applied to humans after traumatic brain injury (e.g., soldiers who have received head trauma in conflict).


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


CURE grant recipients by year:
2016  |  2015  |  2014  |  2013  |  2012  |  2011  |  2010  |  2009  |  2008  |  Older


CURE For questions, please contact Liz Higgins at the CURE office, 312.255.1801, or email

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