Stanford Interdisciplinary Graduate Fellowships (SIGFs)

Many neurological diseases feature the death of neurons, but the mechanisms that mediate cell death in these disorders are unknown. Astrogliosis, the response of a cell-type called “astrocytes” to injury, is common to most diseases of the central nervous system (CNS), and recent studies in our lab suggest that some reactive astrocytes may release a protein that is potently toxic to neurons.

We propose a novel framework for efficient Bayesian cognition called Inference via Abstraction (IvA), which learns to approximate complex world models with simpler abstractions that capture main dependencies, but leverage structure in the prior distribution for efficient inference. We instantiate IvA with a combination of probabilistic graphical models and deep neural networks.

In the course of everyday functioning, animals (including humans) are constantly faced with real-world environments in which they are required to shift unpredictably between multiple, sometimes unfamiliar, tasks. But how brains support this rapid adaptation of decision making schema, and how they allocate resources towards learning novel tasks is largely unknown both neuroscientifically and algorithmically.

Developing a platform of biocompatible nanoparticles that uncage a drug payload upon ultrasound application.

Navigation through an environment to a remembered location is a critical skill we use every day. How does our brain accomplish such a task? Over the last few decades, several lines of evidence have suggested that a brain region called medial entorhinal cortex (MEC) supports navigation by encoding information our location and movement within an environment.

In a process called tiling, homeostatic microglia homogenously organize in a grid-like fashion to achieve efficient surveillance of the brain. The molecular mechanisms underlying tiling are unknown. I hypothesize that microglia use cell-surface proteins to sense density of neighboring microglia, thereby contributing to constant cell-to-cell distances.

A hallmark of the motor system is its ability to execute different skilled movements as the situation warrants, thanks to the flexibility of motor learning. Despite many behavioral studies on motor learning, the neural mechanisms of motor memory formation and modification remain unclear.

Phospholipid dysregulation is implicated in the pathogenesis of lysosomal storage disorders (LSDs). We found that glycerophosphodiesters (GPDs) accumulate in lysosomes derived from Batten disease models, a life-limiting LSD whose pathological mechanism remains elusive. GPDs are the degradation products of glycerophospholipid catabolism by phospholipases.