Reaching the disease before the damage by reshaping APOE4 itself.
I'm a 9th grade researcher working upstream of amyloid and tau, at the protein whose shape decides how early a brain cell becomes vulnerable.
And, in parallel, exploring how to link AI with biology, inspired by brain computer interfaces and work like Neuralink.
Two questions that drive me.
My research centres on the earliest trigger point of Alzheimer's disease, how the APOE4 allele disrupts mitochondrial health, leading to insulin resistance, neuroinflammation, and toxic stress signals that accelerate cognitive decline.
Alongside that, I'm pulled toward a bigger question: how to link artificial intelligence with biology. Inspired by brain computer interfaces and work like Neuralink, I want to help build systems that let computation read, model, and one day support living neural tissue.
Directed biasing of the APOE4 conformational ensemble
An upstream approach to Alzheimer's that works on the shape of the protein itself, rather than on late stage amyloid or tau.
APOE4 isn't one broken protein. It's a moving distribution of shapes.
Across its life inside a cell, APOE4 shifts between states that differ in how they bind lipids and how readily they clump or get stuck. The constricted, poorly lipidated states are the toxic ones, driving oxidative stress, mitochondrial damage, and inflammation. The open, well lipidated states are protective.
My project asks a simple question: if you could gently guide APOE4 toward its safer, open shape, could you lower a cell's vulnerability to Alzheimer's at its earliest origin?
Biasing APOE4 toward an open conformation will improve lipidation and reduce toxic intracellular retention, lowering early cellular vulnerability, and so helping prevent, delay, or partially reverse Alzheimer's disease.
I'm keeping the methods, compounds, and full results private for now while the work develops.
Email me to see the project for yourselfWhere intelligence meets biology.
The questions I care about most live at the seam between living systems and machine intelligence. Inspired by brain computer interfaces and the direction of work like Neuralink, I'm fascinated by the idea of computation that can read, model, and eventually support the brain itself.
Whether it's modelling how a protein behaves, decoding neural signals, or designing better interventions, I believe the next leap in neuroscience comes from pairing biological insight with AI. That belief shapes how I approach every project I take on.
Biology and AI in practice
A parallel project exploring intervention pathways with computational tools.
NeuroShield
A project that combines protein docking, CRISPR based rescue of APOE4, and therapeutic inhibitor design, exploring how computational approaches can open up new intervention pathways for Alzheimer's.
My long term goal is to contribute to next generation therapies that target the root mitochondrial and metabolic failures of Alzheimer's, rather than its late stage symptoms.
Time in the lab
At the neurosciences lab at New York University (NYU) Abu Dhabi, I observed:
- Ongoing research on the circadian rhythm and its link with Alzheimer's.
- Craniotomy on rodents with dementia.
- Fixation of brain tissue in ethanol and sucrose, followed by microscopy.
- Research scholars' own projects in progress.
What's next
I'm planning to return to the NYU lab soon, with the aim of carrying out my own Alzheimer's research work.
I'll be showcasing my research at science fairs in the fall of 2026.
Let's talk research.
Open to mentorship, lab opportunities, and conversations about Alzheimer's, APOE4, and the future of AI in biology.