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Visiting Assistant Professor of Biology Abigail Myers, Gabriela Munoz Rojas '25, and Drake L Gorecki '24 observe mice in the lab.
The cells of our brain, known as neurons, lead early lives of motion. As we develop, they develop too, migrating in our brains to the places they are meant to be. Sometimes, however, their migration becomes disrupted, and the neurons never reach their final destinations. This can cause disorganization in the brain, leading to neurodevelopmental disorders such as epilepsy.

Visiting Assistant Professor of Biology Abigail Myers, along with five students, have spent their summer researching the connection between disrupted neuronal migration and neurodevelopmental disorders, specifically as it relates to the mighty mitochondrion, the powerhouse of the cell.

Mitochondria play an important role in neuronal development, and their disruption is suspected to underlie various neurodevelopmental diseases, Myers said. Using two projects involving mice experiments and pictures of human brain tissue, her summer students researched how disruptions to mitochondrial transport within cells may lead to disturbed neuronal migration, and in turn, neurodevelopmental diseases.

“We’re looking to expand on a phenomenon that people don’t really know much about,” Megan Case ’25 said. “It’s doing something that hasn’t really been done, which is always interesting.”

Drake L Gorecki '24
Drake Gorecki ’24 studies mice in the lab. Photo: Zack Stanek

Case and Cole Rivell ’24 spent their June mornings watching mice run. They placed mice on a spinning rod for two minutes to test how coordination and balance differed between ordinary mice and the genetically modified “knockout” mice.

Importantly, knockout mice have been genetically modified not to produce MIRO-1, a protein that helps facilitate mitochondrial transport in both mice and human neurons. Understanding MIRO-1 can also offer insight into intractable, or uncontrollable, epilepsy because of its association to TRAK, a gene involved in these types of epilepsy in humans.

Case and Rivell saw a difference in coordination between the knockout and control mice, with the knockout mice exhibiting impaired coordination. As the only difference between the knockout mice and the control group was the missing MIRO-1, the researchers can make a connection between deficits in coordination and the missing gene.  

Myers research group
Biology researchers from left, Drake Gorecki ’24, Cole Rivell ’24, Vis. Asst. Bio. Prof. Abigail Myers, Michelle Wu ’25, Gaby Munoz Rojas ’25, Megan Case ’25. Photo: Zack Stanek

By simultaneously looking at sections of mouse brain tissue throughout development, the researchers can also observe how an absence of MIRO-1 affects the organization of neurons, allowing them to more concretely link disorganization in these brains to observed coordinational issues. 

“If we can model neurodevelopmental disorders in mice, then we can think about them in humans as well,” Drake Gorecki ’24 said. 

Gorecki, Gaby Munoz Rojas ’25, and Michelle Wu ’25 also looked at pictures of brain tissue not from mice. They used pictures of human brain tissue obtained through a collaborative project with Jeffrey Golden’s lab at Cedars-Sinai Hospital in Los Angeles. This project examines the mitochondria and neurons in the brain tissues of people who had epilepsy and those who did not. Using an antibody that visibly marks mitochondria, the three can see how incorrect mitochondrial location correlates with neuronal disorganization in brains with epilepsy. 

“Right now, for disorders like epilepsy, we don’t always have an answer as to why they happen or an underlying cause,” Myers said. “Studying this will give us insight into how these disorders develop in humans and inform future treatments.”

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