Morgan Sturgeon
1. Who are you?
I am a 30‐year‐old research scientist from Springfield, Illinois. I obtained my doctoral degree in Molecular Medicine at the University of Iowa in May 2020. After graduation, I decided to stay in Iowa City and accepted a position at Integrated DNA Technologies. My spare time is mostly spent taking care of my dachshund Zenly, visiting with friends and family, and traveling (when a pandemic does not interrupt things).
2. What got you interested in epilepsy research?
I have always been interested in the genetics underlying disease, with the hopes that learning more information can lead to less suffering and loss of life for those diagnosed with poorly understood diseases. I became especially interested in neurodevelopmental and neurodegenerative diseases while doing undergraduate research at Southern Illinois University Edwardsville. After joining a zebrafish lab at the University of Iowa, I realized—like many others before me—that they are an excellent model for joining these two interests together. The genetic tractability of zebrafish and the ability to use them in high‐throughput screens made them a great starting point for studying diseases such as epilepsy and will hopefully lead to better treatments for patients.
3. Explain for our general readership what question your study addressed and how did you go about designing your study?
We have previously published (Brueggeman et al. 2019) our work identifying FDA‐approved compounds capable of inducing a negatively correlative transcriptome change in vitro when compared to the transcriptome profile of hippocampal tissue taken from epileptic patients during resective surgery. In our current study, we sought to test a handful of the most promising compounds (currently used in clinical settings, non‐cost prohibitive, and readily available) on a variety of epilepsy model systems. Starting with a genetics‐induced zebrafish seizure model allowed us to screen these compounds fairly quickly, identify the one(s) that seemed most promising, and then continue testing it in more advanced (ie, mouse brain slice and live mouse) systems.
4. What were the results and how do you interpret your findings?
We began by testing cefoxitin, metformin, pyrantel tartrate, nifedipine, and naltrexone in zebrafish larvae undergoing seizure‐like behavior due to a loss‐of‐function mutation in the scn1Lab gene, which encodes for a sodium channel. In human patients, mutations in this gene often cause Dravet Syndrome. Only naltrexone—an opioid receptor antagonist—reduced the levels of seizure‐like behavior in the larvae, even though metformin, pyrantel tartrate, and nifedipine had shown efficacy against chemically induced seizures in our previous publication. Because of this observed disparity in effectiveness, we wanted to ensure that naltrexone could reduce seizure‐like events in a variety of models. Therefore, we went on to test naltrexone in a chemically induced (via the GABA‐antagonist PTZ) larval zebrafish seizure model, PTZ‐treated mouse hippocampal and neocortical slices, and finally in PTZ‐induced convulsive seizures in mice. We found naltrexone to be effective in each model, both alone and in conjunction with the common anti‐convulsant valproic acid. These findings indicate that naltrexone may be a promising new anti‐convulsant treatment, and that studies in a variety of other models—such as genetically engineered mice—are warranted.
5. What next steps in epilepsy research are you taking and what are your career goals?
Since graduation, my research focus is no longer on epilepsy and is instead centered on improving genomic editing outcomes via CRISPR. However, I hope that this work can be used to improve research on a number of diseases and disorders, including epilepsy. The ability to create cell or animal models that closely mimic human disorders is paramount in the efforts to move therapeutics from bench to bedside. The current trajectory of my career allows me to collaborate and talk with scientists around the world in the hopes of making this goal attainable.
6. What does the epilepsia open prize mean for you, your laboratory, research institute, and your future?
Receiving this award was a great, unexpected honor. Most of my co‐authors remain hard at work in their efforts to better understand and treat epilepsy. I am grateful that this award can help highlight the great work they have done and continue to do. Furthermore, it shows just some of the important research being performed at the University of Iowa, and at the Iowa Neuroscience Institute and Department of Pediatrics in particular.
Read the winning article “The opioid antagonist naltrexone decreases seizure‐like activity in genetic and chemically induced epilepsy models”.