Learning. Building.
Discovering what's possible.
Hi, I'm Jitika.
I'm a neuroscientist, but that's probably the least interesting thing about my story.
My career hasn't been shaped by a carefully planned roadmap. Instead, it's been shaped by questions that refused to leave me alone.
The first one found me during my undergraduate years. I joined a research lab studying protein misfolding in Alzheimer's disease and became fascinated by how something as small as a protein folding incorrectly could have such profound consequences. When I left that lab six months later, I didn't continue studying Alzheimer's. Instead, I spent the rest of my undergraduate years working on Newcastle disease virus for my bachelor's thesis.
Although those projects couldn't have been more different, they shaped me in two important ways.
The first left me with a question I couldn't quite let go of. The second made me realize that what I loved wasn't a particular field of biology, but research itself.
I loved asking questions, designing experiments, getting something wrong, thinking again, and slowly piecing together an answer that hadn't existed before.
When it came time to choose a master's lab, I could have continued working on viruses. I already knew the techniques, the field, and the people. Instead, I returned to the question that had stayed with me for almost two years. Not because I had a plan to become an Alzheimer's researcher, but because I was still curious.
It took me years to realize that I wasn't returning to a topic. I was returning to a way of thinking.
As my research evolved, so did the questions I was asking.
Protein aggregation led me to lipid metabolism.
Lipid metabolism led me to neuroimmune interactions.
Those questions eventually expanded into human disease models, therapeutic development, and building better ways to study disease.
People often see these as different projects. I don't. I think I just kept zooming out.
During my PhD, another realization emerged. The part of science I enjoyed most wasn't only discovering new biology.
It was building the things that made discovery possible: experimental models that better capture disease, image analysis pipelines that extract more meaningful information, and collaborations that bring together people with completely different ways of thinking.
Building has become the lens through which I approach science, and I realized that I'm not limited by the skills I have today. I'm limited only by the problems I care deeply enough to learn for.
If a question matters to me, I'll learn whatever it takes to answer it. Biology. Imaging. Computational methods. AI. The tools have changed throughout my career, but my approach hasn't.
There's another pattern that's impossible for me to ignore.
Almost every meaningful opportunity I've had began because someone believed in me before I had fully earned it.
An undergraduate advisor who trusted me with real responsibility.
A professor who eventually replied to the persistent emails of an overly enthusiastic master's student.
A former lab member who introduced me to the lab that would completely change the direction of my PhD.
Friends who answered late-night phone calls when I had just moved halfway across the world.
Parents who gave me the freedom to build a life around what genuinely excited me.
Those experiences changed me just as much as the science did. They taught me that meaningful work is rarely the product of one person. It comes from people who challenge one another, trust one another, and build something together that none of them could have built alone. That's the kind of scientist, collaborator, and teammate I hope to become.
This website exists because a CV can only tell part of the story.
It can tell you what I've done, but it can't tell you how I think, what kinds of questions excite me, or why I care so deeply about building. I wanted one place where those parts of me could exist alongside the science.
If something here resonated with you, whether it was a scientific question, a shared curiosity, or simply a way of thinking, I'd genuinely love to hear from you.
After all, every meaningful chapter of my own story began with a conversation.
Education
Undergraduate & Graduate Degrees
Ph.D. in Chemistry (Integrated Neuroscience)
M.S. in Biochemistry and Cell Biology
B.Tech. in Biotechnology
Executive Education
microMBA
Completed an intensive executive education program combining business strategy, innovation, and leadership principles. Supported by professional grant award from Purdue Graduate Student Government, demonstrating institutional recognition of the program's value. This education bridges scientific expertise with business acumen, preparing for leadership roles that translate fundamental research into therapeutic impact.
Research Internship
Summer Research Internship
Completed a 3-month internship at the University of Nottingham, Derby Hospital with Dr. Wayne Carter.
How does altered lipid metabolism reshape immune responses in Alzheimer's disease?
Alzheimer's disease is accompanied by profound changes in lipid metabolism, yet whether these changes actively drive disease or simply reflect it has remained unclear. To address this question, I developed complementary mouse and human iPSC-derived models, quantitative imaging approaches, and chemical biology tools to investigate how disrupted lipid metabolism contributes to neurodegeneration. My research has followed two complementary directions.
In my first project, I identified DGAT2 as a key regulator of lipid droplet accumulation in microglia. By comparing pharmacological inhibition with targeted protein degradation (PROTACs), we found that eliminating the protein, rather than inhibiting its enzymatic activity, restored microglial homeostasis and reduced Alzheimer's pathology in aged mouse models, highlighting targeted protein degradation as a promising therapeutic strategy.
Building on these findings, I investigated how altered lipid metabolism reshapes adaptive immunity through lipid antigen presentation, uncovering a potential link between lipid dysregulation and neuroinflammation in Alzheimer's disease.
Together, these studies suggest that disrupted lipid metabolism is not merely a consequence of disease but an active driver of neuroinflammation and a promising avenue for therapeutic intervention.
How do disease-causing mutations alter the earliest stages of amyloid-β aggregation in cerebral amyloid angiopathy?
Cerebral amyloid angiopathy is driven by the accumulation of amyloid-β within cerebral blood vessels, yet the Dutch and Iowa mutations produce distinct disease phenotypes despite differing by only a single amino acid. By characterizing the earliest stages of amyloid assembly, I identified a transient β-hairpin intermediate unique to the Iowa mutation that redirects aggregation into an alternative pathway. These findings reveal how subtle structural differences can profoundly influence disease pathology.
How do Newcastle disease virus proteins reshape host cell biology?
Viruses rely extensively on host cells to replicate, but the ways viral proteins interact with cellular machinery are often poorly understood. Using Saccharomyces cerevisiae as a model system, I investigated how the Newcastle disease virus nucleocapsid and matrix proteins influence intracellular organization, organelle morphology, and cellular stress responses. This work provided mechanistic insight into virus-host interactions while introducing me to cell biology, microscopy, and experimental research as an undergrad.
Questions That
Keep Me Curious
Science moves forward because someone keeps asking the next question. These are a few of the questions I find myself thinking about most often.
Why do patients with the same diagnosis respond so differently to the same therapy?
Disease labels often hide remarkable biological diversity. I'm fascinated by the challenge of identifying the molecular mechanisms that distinguish one patient from another, with the hope of developing therapies that are guided by biology rather than diagnosis alone.
How can we build experimental models that better reflect human brain aging and diseases?
Our ability to understand disease is fundamentally limited by the models we use to study it. I'm interested in developing human-relevant experimental systems that better capture the biology of aging and neurodegeneration, enabling deeper mechanistic insight and more predictive translational research.
Why do so many promising therapies fail despite targeting the "right" biology?
Neurodegenerative diseases arise from complex, interconnected biological processes. I want to understand when, where, and how we should intervene, and whether combining complementary therapeutic strategies can lead to more durable and meaningful outcomes.
How can we combine human biology, experimental science, and AI to build better medicines?
Building AI-based image analysis tools was one of the experiences that most changed the way I think about AI in science. It showed me that it's not just a way to automate analysis, but a powerful partner in discovery when thoughtfully integrated with experimental research. Since then, I've been fascinated by the potential of combining AI with experimental biology to build smarter tools, ask better questions, and accelerate scientific discovery.
Let's Connect
Thanks for stopping by. If something on this website sparked a question, an idea, or simply resonated with you, I'd love to hear from you. Great ideas often begin with simple conversations, and the best ones are built together. Let's start one.
