Funded Projects

We propose a new line of research whose goal is to examine the druggability of a protein-protein interface involving ApoE, an apolipoprotein whose gene variants represent the strongest genetic risk factor for AD.

People with Parkinson’s Disease (PD) have different types of bacteria in their guts compared to people without neurological diseases. We will study which gut bacteria for people with PD to gain a better understanding of how gut bacteria contribute to inflammation in the body and in the brain or people with this condition. 

We propose to apply mass spectrometry techniques to measure BHB-Phe and other KD metabolites in children undergoing KD for refractory epilepsy at Stanford. Further, in a mouse model of refractory genetic epilepsy, we will compare targeted BHB-Phe treatment to full KD treatment using transcriptomics, EEG assessment of seizures and cognitive testing.

Why do all our brains mature and age in different ways, leading to different cognitive and behavioral outcomes? We envision a novel method that “copies” the information from the RNAs made by the neurons to sensor RNAs we artificially introduce into live animals. 

In this study, we aim to (i) perform a feasibility study to determine the acceptance and feasibility of performing such recordings in the AN and ARFID eating disorders population and (ii) test the hypothesis that the electrophysiologic monitoring of the brain and stomach is associated with a clinically validated behavioral measure of interoception involving water distention of the stomach.

This proposal brings together faculty with this diverse expertise to develop the first gold standard test of auditory-vocal affect. Once developed, validated, and normed, we will deploy this test in the clinical context of autism to quantify impairments and direct neurobiological investigation.

Schwann cells (SCs) sort and myelinate peripheral axons, and impairments in either process can cause long-term disability. There are no therapeutic strategies for targeting SC dysfunction, underscoring the need to investigate mechanisms of sorting and myelination. Both processes require highly motile SC cytoplasmic protrusions, but the basis of this motility is unclear.

Absence epilepsy is a form of pediatric epilepsy which causes seizures with brief lapses in awareness. Electron microscopy results in a murine model of absence epilepsy support the hypothesis that maladaptive myelination plays a role in disease progression.

Many neurological injuries and diseases such as brainstem stroke and Amyotrophic Lateral Sclerosis (ALS) result in severe speech impairment, drastically reducing quality of life. Recent progress in brain-computer interfaces (BCI) has allowed these individuals to communicate, but performance is still far lower than typical spoken conversation speeds.

We will comprehensively define the gene network associated with mitochondrial dysfunction in Parkinson's disease using a cutting-edge technology, CRISPR, to understand how these nerve cells die in PD and how we can reverse the cell death to treat the disease.

Maternal infection is linked to increased risk of neurodevelopmental disorders such as autism and schizophrenia. This proposal examines how virus-associated cytokines, specifically interferons, affect human neurons modeled in brain organoids or studied directly in fetal brain samples.

Mental illnesses like bipolar disorder affect millions of people around the world, but early symptoms are often difficult to detect. Working across the disciplines of clinical psychology, communication, and computer science, my research will develop a novel computational tool to identify signals of mania and depression in real-time.

Traumatic brain injury (TBI) has become a global health hazard. If undetected, the brain damage of TBI can accumulate, calling for better TBI modeling and warning systems. TBI modeling involves three stages: head impact kinematics, brain deformation, and injuries.

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.