Nancy Ahuja is a postdoctoral researcher at the University of Oxford. She investigates extracellular vesicle communication between astrocytes and dopaminergic neurons to uncover key mechanisms driving neurodegeneration in Parkinson's disease. In this Postdoc Portrait interview, she shares the importance of her work and what she hopes her research will accomplish.
Decoding Neuron-Astrocyte Communication in Parkinson's Disease
Q | What scientific problem are you trying to solve?
Parkinson's disease is often thought of as a disease that primarily affects dopamine-producing neurons, but growing evidence suggests that the surrounding support cells, called astrocytes, also play a crucial role in disease progression. Despite this, we still do not fully understand how these two cell types communicate or how that communication changes in Parkinson's disease. My research aims to address this gap by studying induced pluripotent stem cell (iPSC)-derived dopaminergic neurons and astrocytes generated from healthy individuals and patients carrying alpha-synuclein-related disease mutations. I focus on extracellular vesicles (EVs), tiny membrane-bound particles that cells use to exchange molecular signals. By comparing the cargo carried by EVs released from healthy and patient-derived cells, I hope to uncover how disrupted neuron-astrocyte communication contributes to neurodegeneration. Ultimately, this work could help identify new biomarkers and therapeutic targets that preserve neuronal health and slow the progression of Parkinson's disease.
Q | What drew you to this field?
I first became interested in Parkinson's disease during my PhD, where I studied how nuclear receptors regulate endoplasmic reticulum stress using cell lines and animal models. While this gave me a strong foundation in disease mechanisms, I often wondered how well these models reflected what happens in patients. During my postdoctoral research, I was introduced to iPSC technology, and it completely changed how I thought about studying neurodegenerative disease. The ability to generate patient-specific brain cells while preserving an individual's genetic background was fascinating because it offered a way to investigate disease processes in a much more physiologically relevant human model.
Initially, my work focused on dopaminergic neurons, but I became increasingly interested in the role of astrocytes. Rather than simply supporting neurons, astrocytes actively shape neuronal health, communication, and survival, and growing evidence suggests they play a key role in Parkinson's disease. Exploring how neurons and astrocytes communicate, particularly through extracellular vesicles, felt like a natural progression of my research. I am motivated by the opportunity to better understand these interactions and uncover mechanisms that could ultimately lead to new therapeutic strategies for Parkinson's disease.
Targeting Cellular Networks for Therapeutic Breakthroughs
Q | What’s one thing you learned from your research that you didn’t expect?
One of the biggest surprises for me has been realizing how much of Parkinson's disease is shaped by the cells surrounding neurons. I initially thought of astrocytes as support cells whose main role was to maintain a healthy environment for neurons. Through my research, I have learned that they are far more dynamic than I expected. Astrocytes actively communicate with neurons, respond to stress, and can influence whether neurons survive or degenerate. Studying extracellular vesicles has reinforced this idea, showing that cells are constantly exchanging molecular information in ways we are only beginning to understand. This has changed how I think about neurodegenerative disease, not as a problem of a single vulnerable cell type, but as a dysfunction of an entire cellular network. It has made me appreciate the importance of studying interactions between different cell types, rather than focusing on neurons alone, if we want to fully understand Parkinson's disease.
Q | If your research succeeds, what could it change for science or society?
Identifying disease-associated changes in extracellular vesicle cargo could provide new biomarkers for earlier and more accurate diagnosis, as well as novel targets for therapeutic intervention. This work could contribute to the development of strategies that not only aim to replace lost neurons, but also preserve the supportive environment needed to maintain neuronal health. Ultimately, this could open new avenues for slowing or modifying disease progression, improving quality of life for patients, and reducing the long-term societal burden of Parkinson's disease.
Q | What question are you most excited to answer next?
I am especially interested in identifying whether specific changes in vesicle cargo from patient-derived cells can actively drive neurodegeneration or, conversely, support resilience in neurons. If we can pinpoint these signals, it may be possible to shift the balance from a toxic to a protective environment.
Responses have been edited for length and clarity.
Are you a researcher who would like to be featured in the “Postdoc Portraits” series? Send in your application here.
