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.
Core capabilities built across my research journey



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.
Completed a 3-month internship at the University of Nottingham, Derby Hospital with Dr. Wayne Carter.
I am a scientist who builds systems to answer questions that sit at the intersection of disease biology and therapeutic development.
My PhD focused on understanding how disrupted lipid metabolism drives neuroinflammation in Alzheimer's disease. To do that, I built the experimental infrastructure myself, establishing the lab's first iPSC-derived human cellular models, developing quantitative imaging pipelines, and running end-to-end studies in mouse models from drug delivery through tissue analysis.
What I found was that lipid dysregulation isn't a side effect of disease. It actively impairs the brain's immune cells and connects to neuroinflammation through a pathway that hadn't been explored in this context before. That finding shifted how we think about therapeutic entry points in Alzheimer's disease and pointed toward a new class of intervention strategies.
I work across scales, from molecular mechanisms to cellular systems to in vivo validation, and I bring both the scientific judgment to ask the right questions and the technical range to answer them across platforms.
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.
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.
Science moves forward because someone keeps asking the next question. These are a few of the questions I find myself thinking about most often.
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.
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.
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.
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.
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.