Postdoctoral Research and Training Fellowship
The Postdoctoral Research Fellowship develops academic physicians and scientists committed to research related to epilepsy. Applications are considered equally from individuals interested in acquiring experience either in basic laboratory research or in the conduct of human clinical studies. Physicians or Ph.D. neuroscientists who desire postdoctoral research experience are eligible to apply.
Postdoctoral Research Fellowships fund basic laboratory research and human clinical studies. Fall grants totaling $495,000 will support research into:
- Sudden Cardiac Death In a Severe Form of Childhood Epilepsy: Mice & Men;
- Defining ECoG Resting State Networks Associated With Focal Epilepsy;
- A Role for Interleukin-6 in Epileptogenesis;
- The pathogenic role of activated microglia in epilepsy;
- Restoring Consciousness during seizures using optogenetic stimulation;
- Reelin signaling mediates aberrant neurogenesis in temporal lobe epilepsy;
- Investigating the mechanism of stress induced seizure susceptibility;
- Detection & Prediction of Human Seizures using Intracortical Neural Signals;
- Screening for seizure modifiers in Drosophila knock-in model of SMEI;
- mTOR, epilepsy and synaptic transmission;
- Innate and Adaptive Immunity in Epileptogenesis of Childhood Epilepsy.
Sudden Cardiac Death in a Severe Form of Childhood Epilepsy: Mice & Men
David Scott Auerbach, PhD Postdoctoral Research FellowThe Regents of the University of Michigan Ann Arbor, MI, United States
Patients with Dravet Syndrome experience uncontrollable electrical disturbances in the brain, seizures. Many young patients die suddenly, yet often the cause of death remains unknown. Seizures can be traced back to mutations in one of the sodium channel genes. Interestingly, these mutated sodium channels are also present in the heart. Therefore, I am interested in testing whether, similar to the brain, mutated sodium channels cause electrical disturbances in the heart, called arrhythmias. Arrhythmias may provide an explanation for sudden death in patients with Dravet Syndrome. The mechanism(s) for the initiation of these electrical disturbances in the heart will be explored.
Funding for this grant was supported by the American Epilepsy Society and Eisai, Inc.
Defining ECoG Resting State Networks Associated With Focal Epilepsy
Sarah Bandt Resident Physician Washington University in St. Louis St. Louis, MO, United StatesEpilepsy affects 3 million Americans at an estimated yearly cost of $15.5 billion 1/3 of these patients never achieve seizure control with medication alone.Surgery may help some of these patients.There have not been many recent advances in the way we treat epilepsy with surgery.The purpose of this project is to analyze seizures directly from the surface of the human brain to try to better understand the relationships between the cells causing the patient's seizures and the surrounding brain tissue to guide surgical resections to maximize seizure control with minimal injury to normal brain function.
Funding for this grant was supported provided by the American Epilepsy Society.
A Role for Interleukin-6 in Epileptogenesis
Jeff Boychuk Postdoctoral ScholarUniversity of Kentucky Research Foundation Lexington, KY, United States
Traumatic head injury is a leading cause of acquired temporal lobe epilepsy (TLE). This work intends to help understand the process whereby brain injury promotes the development of chronic seizure disorders. Head injury results in massive inflammatory responses in the brain. This proposal examines how the body's natural inflammatory response to brain injury may influence chronic changes in brain function leading to epilepsy. The focus here is whether one inflammatory protein, Interleukin-6, signals brain cell networks to become permanently in a manner consistent with the development of TLE. Experiments here study how Interleukin-6 affects both excitatory and inhibitory brain networks.
Funding for this grant was supported by the American Epilepsy Society and Lennox & Lombroso Trust for Epilepsy Research and Training.
The pathogenic role of activated microglia in epilepsy
Zhihong Chen Postdoctoral fellow Cleveland Clinic Foundation Cleveland, OH, United StatesEpilepsy is a persistent and devastating neurological disease characterized by repeated seizures. It is among the least understood chronic disorders and current medications are only effective in a fraction of the patients. Here, I propose to inspect brain inflammation, recently found happening hand-in-hand with epilepsy, for its potential roles in the development of this disease. Well established animal models and modern technologies will be used to understand the underlying mechanisms of epilepsy-associated inflammations. This work will help advance our knowledge about epilepsy and offer insight into the designing of effective treatment.
Funding for this grant was supported by the American Epilepsy Society and Sunovion Pharmaceuticals, Inc.
Restoring consciousness during seizures using optogenetic stimulation
Moran Furman, Ph.D. Postdoctoral AssociateYale University New Haven, CT, United States
Loss of consciousness in epilepsy is a major burden for patients and society. Even small seizures in brain regions devoted to memory can cause loss of consciousness, and currently, there are no effective therapies to prevent this debilitating side-effect of epilepsy. Seizures in rats, like in humans, cause impaired consciousness. We will use two brain stimulation techniques – electrical stimulation, and optogenetics, a novel technique based on activation of neurons by laser light – to prevent loss of consciousness in epileptic rats. This research will hopefully pave the way for novel therapies to prevent loss of consciousness during seizures in humans.
Reelin signaling mediates aberrant neurogenesis in temporal lobe epilepsy
Matthew Joseph Korn, Ph.D. Postdoctoral Research FellowThe Regents of the University of Michigan Ann Arbor, MI, United States
Mesial temporal lobe epilepsy is a common and often intractable form of epilepsy. Many of the pathological changes take place in the hippocampus where the disruption of the circuit results in persistent hyperexcitability. Adult-born neurons are prone to developing abnormalities that may contribute to chronic spontaneous seizures. Despite advances in understanding the pathogenesis of the disease, few therapeutic targets are available. This proposal investigates how changes to the reelin signaling pathway, known to be disrupted in mTLE, impact the development of immature neurons in the hippocampus. If spontaneous seizures develop, it would offer reelin signaling as a target for treatment.
Investigating the mechanism of stress induced seizure susceptibility
Georgina MacKenzie, Ph.D. Postdoctoral AssociateTufts University Boston, MA, United States
The majority of epilepsy patients report that stressful situations exacerbate their seizures. However, the complex relationship between stress and epilepsy is still not fully understood. This project investigates a novel mechanism linking stress to increased neuronal excitability and seizure susceptibility with the goal of identifying new therapeutic targets for the treatment of epilepsy.
Funding for this grant was supported by the American Epilepsy Society and Sunovion Pharmaceuticals, Inc.
Detection & Prediction of Human Seizures Using Intracortical Neural Signals
Yun Sang Park Postdoctoral Research Associate Brown University Providence, RI, United StatesOne of the most debilitating aspects of epilepsy is the seemingly unpredictable nature of seizures.Reliable early-detection or even prediction of seizures could bring tremendous benefits to people with epilepsy, including a significant improvement in therapeutic possibilities.The project aims at developing and testing a novel framework for early detection and prediction of seizures in people with epilepsy using experimental intracortical neural signals.The long-term goal is to develop a closed-loop system for seizure warning, prediction, and control and ultimately to conduct a human pilot clinical trial with the system.
Screening for seizure modifiers in a Drosophila knock-in model of SMEI
Lei Sun Postdoctoral Fellow The Regents of the University of California (Irvine) Irvine, CA, United StatesDravet syndrome, also known as severe myoclonic epilepsy of infancy (SMEI), is a catastrophic form of intractable epilepsy that begins in infancy. Over 300 different mutations in SCN1A sodium channel gene have been linked to SMEI, and the limited ability to evaluate disease mechanisms hampers development of effective therapeutics. We will use a Drosophila model of human SMEI to study the underlying mechanisms of SMEI and to screen for novel therapeutic targets. The Drosophila models of SMEI provide a rapid, low cost platform for categorizing SMEI mutations by function and developing therapies for personalized treatment.
Funding for this grant was supported by the American Epilepsy Society and Sunovion Pharmaceuticals, Inc.
mTOR, epilepsy and synaptic transmission
Matthew Weston, Ph.D. Postdoctoral FellowBaylor College of Medicine Houston, TX, United States
In both humans and mice, mutations in genes that control mammalian target of rapamycin (mTOR) signaling lead to epilepsy. In some cases of epilepsy, changes in how nerve cells communicate with each other are thought to be a cause. Discovering ways in which communication between nerve cells are altered in mice that have mutations affecting mTOR signaling will lead to a better understanding of the development of epilepsy.
Funding for this grant was supported by the American Epilepsy Society and Lennox & Lombroso Trust for Epilepsy Research and Training.
Innate and Adaptive Immunity in Epileptogenesis of Childhood Epilepsy
Dan Xu Postdoctoral Trainee Northwestern University-Chicago Campus Chicago, IL, United StatesThe goal of this project is to determine if the presence of inflammation in the seizing brain of young children would increase the likelihood of recurrent seizures, and eventually leads to epilepsy. Approximately 1 in every 25 children will have at least one febrile seizure, which is convulsion brought on by a fever. One-third of these children will have additional febrile seizures, which is intrinsically associated with inflammation. This project, therefore, adopts a mouse model that recapitulates human epilepsy to study whether manipulation of the inflammation can prevent the development of epilepsy and to identify novel targets for improved therapy.
