Stanford Interdisciplinary Graduate Fellowships (SIGFs)

Constipation and diarrhea, caused by aberrant water absorption in the colon, impose substantial health burdens. The enteric nervous system (ENS) harbors a specialized circuit for water absorption, the secretomotor/vasodilator circuit, but its role in the proximal colon remains poorly understood.

The medial entorhinal cortex (MEC), the brain’s “inner GPS”, contains an internal map of external space. Rather than representing a static spatial map, however, MEC neurons can spontaneously switch between multiple maps (Low et al., 2021). In this project, we will investigate if spontaneous map switches reflect changes in an animal’s latent internal state.

Understanding representational drift—the brain’s evolving representation of its environment—is pivotal to gaining insights into neural computation. Despite its significance, the study of representational drift has been constrained by the scarcity of suitable datasets and methods.

Parkinson’s disease (PD) is a complex, heterogeneous neurodegenerative disorder whose prevalence is increasing rapidly. Not only do patients experience motor symptoms, but many experience debilitating nonmotor symptoms caused by peripheral degeneration in the autonomic nervous system, including atrophy of the vagus nerve, and the enteric nervous system.

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.