As an undergraduate, Mitch Murdoch was a rare science and humanities double major at Yale University, specializing in both English and molecular, cell, and developmental biology. Now, as a Ph.D. student in the Massachusetts Institute of Technology’s Department of Brain and Cognitive Sciences, he sees first-hand the obvious ways English education has broadened his horizons as a neuroscientist.

“One of my favorite parts of the English language was trying to explore interiority, and how people go through very complex experiences in their heads. explains Murdock. “I was excited to try to bridge the gap between the internal experience of the world and the actual biological substrate of the brain.”

Although he can see those connections now, it wasn’t until after Yale that Murdoch became interested in brain science. As an undergraduate, he was in a traditional molecular biology lab. He intended to remain there after graduation as a research technician. Luckily, he says his advisor, Ron Breaker, encouraged him to explore this area. That’s why Murdoch ended up in a new lab run by Conner Liston, an associate professor of medicine at Weill Cornell Medicine, studying how factors such as stress and sleep modulate the modeling of brain circuits. rice field.

It was in Liston’s lab that Murdoch first came into contact with neuroscience and began to see the brain as the biological basis for the philosophical questions about experience and emotion that interested him. “Really in his lab, I thought, ‘Wow, this is so cool.

While working as a research technician, Murdoch examined the effects of chronic stress on brain activity in mice. Specifically, in the hope that a better understanding of how ketamine works will help scientists find safer alternatives to abuse-prone fast-acting antidepressants. I was interested in a certain ketamine. He looked at dendritic spines. Dendritic spines are small organelles attached to neurons that help transmit electrical signals between neurons and provide the physical basis for the storage of memory. His findings suggest that ketamine works by restoring dendritic spines that can be lost after periods of chronic stress, explains Murdoch.

After three years at Weill Cornell, Murdock decided to pursue a doctorate in neuroscience, hoping to continue some of the research he started at Liston. He chose his MIT because of William R. (1964) and Linda R. at the Picower Institute for Learning and Memory, where his research on dendritic spines was carried out in the laboratory of Elly Nedivi, a young professor of neuroscience. because

Again, the opportunity to explore broader interests happened to lead Murdoch to a new passion. During his lab rotation at the start of his doctoral program, Murdoch spent time chaperoning doctors who were treating Alzheimer’s patients at Massachusetts General Hospital.

“We all know there is no cure for Alzheimer’s disease. It was a wake-up call.”

After that experience, Murdoch strategically planned the remaining lab rotations, eventually settling in the lab of Lihuei Tsai, Picower Professor of Neuroscience and Director of the Picower Institute. Over the past five years, Murdock has collaborated with Tsai on various areas of Alzheimer’s research.

For example, in one project, members of the Tsai lab demonstrated how certain types of non-invasive light and sound stimulation induce brain activity that can ameliorate memory loss in a mouse model of Alzheimer’s disease. I was. Scientists believe that tiny movements of blood vessels during sleep pump spinal fluid into the brain, which in turn flushes out toxic metabolic waste products. It has been suggested that it may promote memory loss and wash away waste products that can exacerbate amnesia.

Much of his research focuses on the activity of single cells in the brain. Are certain neurons or neuron types genetically prone to degeneration, or do they randomly collapse? Certain subtypes of cells appear to malfunction in the early stages of Alzheimer’s disease. How do changes in blood flow in vascular cells affect degeneration? All of these questions will help scientists better understand the causes of Alzheimer’s disease and ultimately Murdoch believes it will lead to the development of cures and cures.

To answer these questions, Murdock relies on a new single-cell sequencing technique that he says has changed the way we think about the brain. “This was a big advance for the field because we know there are different types of cells in the brain, and we think they can have different effects on Alzheimer’s risk.” ‘he says Murdock. “You can’t think of the brain as just neurons.”

Murdoch says that such a “big picture” approach — thinking of the brain as a collection of different types of cells all interacting — is a central tenet of his research. . To examine the brain in the kind of detail the approach calls for, Murdoch collaborated with Ed Boyden, Professor of Neurotechnology Y. Eva Tan, Professor of Bioengineering and Brain and Cognitive Sciences at MIT, Howard Hughes Medical Institute. Researcher and member of the McGovern Institute for Brain Research and the Koch Institute for Integrated Cancer Research at MIT. By working with Boyden, Murdoch was able to use new technologies such as extended microscopy and gene-encoded sensors to aid research.

This kind of new technology has helped open up the field significantly, he adds. “It’s a very cool time for neuroscientists, because now is the golden age of studying the brain, thanks to the tools available today.” That’s true, an area Murdoch says he wants to continue after graduation, including the newly understood relationship between the immune system and Alzheimer’s disease.

But for now, Murdoch’s focus is on review papers summarizing some of the most recent research. “It’s crazy,” he admits, but couldn’t be happier to be in the middle of it. , is very exciting.”