Q | Write a brief introduction to yourself including the lab you work in and your research background.
I am Priya Prakash, a cellular and molecular neurobiologist in Shane Liddelow’s Lab at NYU Grossman School of Medicine. My research focuses on how glial cells (astrocytes, microglia, and oligodendrocytes) become dysfunctional and drive neurodegeneration. Currently, I am researching how oligodendrocyte dysfunction contributes to tissue pathology in X-linked dystonia-parkinsonism, a rare neurodegenerative movement disorder.
Q | How did you first get interested in science and/or your field of research?
As an undergraduate in India, I had very limited opportunities for laboratory training, which left me eager to gain hands-on research experience. This motivation led me to move to the United States for my master’s degree, where I worked for the first time in a protein biochemistry lab. That experience confirmed my passion for discovery at the bench and inspired me to pursue full-time research as a doctoral student.
During my Ph.D. training in the interdisciplinary life sciences program at Purdue University, I rotated through labs in diverse fields including biomedical engineering, neuroscience, and cancer biology. I ultimately joined Gaurav Chopra’s lab, where I was encouraged to follow my curiosity and develop independent projects. Around this time, I was introduced to the work of Dr. Ben Barres, a pioneer in neuroscience and glial biology. Reading about his scientific journey and groundbreaking studies on glia sparked my fascination with microglial biology. This inspiration led me to combine chemistry and neuroscience to study how glial cells respond to amyloid-β pathology in Alzheimer’s disease, a focus that continues to shape my career today.
Q | Tell us about your favorite research project you’re working on.
On a small island called Panay in the Philippines, a subpopulation of men develops progressive motor symptoms resembling dystonia and Parkinsonism. The cause of this devastating disorder, called X-linked dystonia-parkinsonism (XDP), is an insertion of a mobile non-coding genetic element known as an SVA retrotransposon into the ubiquitously expressed TAF1 gene. Because this retrotransposon is unique to humans, researchers have long struggled to model and study the disease pathophysiology.
In collaboration with Jef Boeke’s lab at NYU, we developed a novel humanized XDP mouse model that introduces the human-specific SVA retrotransposon into TAF1, faithfully reproducing key features of the disorder. Using this model, I uncovered an unexpected role for oligodendrocytes (the myelin-producing glial cells) in XDP pathology. Consistent with our mouse findings, analyses of human postmortem XDP brain tissue revealed profound myelin abnormalities, highlighting white matter dysfunction as a major contributor to disease progression.
This project is especially meaningful to me because it bridges molecular neuroscience with a rare human disorder, offering mechanistic insight and potential therapeutic relevance. Most importantly, it reflects what excites me most about science: following where the data leads, even when it takes me into entirely new directions, such as uncovering oligodendrocyte biology after years of studying microglia and astrocytes.
Q | What has been the most exciting part of your scientific career/journey so far?
The most exciting part of my scientific journey has been discovering results that challenge my original hypotheses and following the data wherever it leads. When I began graduate school in a chemistry lab, I never imagined I would end up studying glial cells in the brain. Yet curiosity drew me toward neuroimmunology, where I investigated how microglial dysfunction contributes to Alzheimer’s disease pathology. For my postdoc, I shifted focus to astrocytes, only to be surprised once again when my experiments revealed that oligodendrocytes are key players in a rare neurodegenerative disorder. Today, I am pursuing this direction using a humanized mouse model we developed, which allows me to study the cellular basis of this disease in ways that were never possible before.
What excites me most is that science is never a straight path. Each unexpected turn has opened new perspectives and challenges, and I’ve learned to embrace flexibility and curiosity as strengths. Rather than confining me to a single niche, science has allowed me to explore the many ways glial cells shape brain. That unpredictability—the joy of discovery and the thrill of being led to new directions by data—is what makes this journey so deeply rewarding.
Q | If you could be a laboratory instrument, which one would you be and why?
I’d be the mighty old pipette! It may not be as flashy as a microscope or as dramatic as a flow cytometer, but it’s the quiet workhorse of science—reliable, precise, and essential to almost every experiment. That’s how I like to approach research: steady, dependable, and always ready to put in the work, drop by drop, to build something bigger. To me, the pipette embodies patience, persistence, and progress—one measured step at a time!
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