Funded Projects

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.

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.

Understanding the relationship between structure and function in the human brain is a key interest in neuroscience. In recent years the focus is turning to understanding the role of the white matter in human cognition, brain function and neurological disorders.

Electrodes implanted in the brain have great potential, with applications in neurodegenerative disease, brain-computer interfaces, and more. However, the presence of electrodes in brain tissue causes a response known as gliosis, in which a scar forms around the electrode, reducing its effectiveness and access to neurons.

Stroke is the main cause of adult disability; 80% of survivors sustain motor (movement) deficits that interfere with activities of daily living. There exists no proven therapeutic strategy for motor recovery of the upper extremity following stroke.

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.

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.

Yi Lui's project aims to use deep brain microstimulation (DBMS), which causes even less brain damage and has higher spatial resolution than DBS, for memory recovery.

Dr. Darian Hadjiabadi aims to identify higher-order features of neuronal circuits responsible for seizure initiation and propagation by quantifying mesoscale-network reorganization in genetic models of zebra sh that faithfully recapitulate seizure dynamics in humans.

Dr. Brandon Jay Bhasin will use engineering principles from modern control theory, experimental neuroscience and computational neuroscience to significantly advance understanding of how feedback driven plasticity in a tractable neural circuit is orchestrated across multiple synaptic sites and over various timescales so that circuit dynamics are changed to improve performance.

The project aims to alleviate this bottleneck by developing a weak supervision system that optimally deals with time-series data and takes advantage of multiple data modalities.

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

Behavioral state—such as alertness or exhaustion—dramatically impacts how our brains function. Yet, in spite of the key role that it plays in cognition, how behavioral state influences brain function remains a central mystery in neuroscience.

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.

Although ultrasonic neurostimulation has the potential to outperform traditional treatments for many debilitating neurological disorders, it remains unclear how ultrasound affects nervous system activity on the molecular level.

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.

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.

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.

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.