Research

My research aims to understand how the nervous system regulates hemodynamics, and how that regulation can be restored after spinal cord injury. My work runs from circuit-level recording in animal models to measurement in people, and I build the instrumentation each question requires.

Closed-loop neuromodulation for hemodynamic stability

Epidural electrical stimulation can raise blood pressure after spinal cord injury, but open-loop stimulation cannot respond to what the body actually needs. I develop closed-loop systems that decode hemodynamic state directly from brainstem sympathetic circuits and use that signal to gate stimulation in real time. Building the decoder requires a mechanistic account of how these circuits encode pressure, so each system is both a therapy and a probe: what restores blood pressure control also reveals the circuit mechanisms that normally maintain it.

Digital phenotyping of autonomic dysfunction

Hypotension after spinal cord injury is under-recognized, in part because standard clinical assessment is resource-intensive and carries risk. I validated the hypotension symptom domain of the ADFSCI questionnaire as a patient-reported measure, using both physiological testing and a global dataset of patient responses. This extends the same questions into clinical and real-world settings where continuous physiological monitoring is not practical.

Chemoreflex control of blood pressure after spinal cord injury

Breathing and blood pressure are regulated together. Rising CO2 normally drives a coordinated sympathetic response, but spinal cord injury interrupts the descending pathways that carry that drive to the circulation. I use controlled respiratory challenges to dissect two mechanisms that CO2 engages at once: sympathetic drive descending from the brainstem, and local coupling between neural activity and perfusion within the cord. The work runs in rodents and in a large-animal pig model, whose anatomy and hemodynamics sit closer to the human case, and aims to establish which mechanism sets the ceiling on recovery.

Memory circuits in Drosophila

During my PhD at the Friedrich Miescher Institute, I showed that separable dopaminergic pathways gate the recovery of true memories and the formation of false ones from forgotten information. Combining two-photon calcium imaging with behavioral paradigms, I found that forgotten memories persist as silent traces in behaviorally neutral circuits, and that reminders can either reinstate them faithfully or distort them. The work established memory recovery as a reconstructive process rather than a simple replay.

Whole-Brain Imaging and Computational Methods

A constant across these projects is building the measurement system the question requires. I contributed to extended light field microscopy (XLFM), which captured whole-brain activity at neuronal resolution in freely behaving zebrafish and recorded the complete prey capture sequence for the first time. In earlier work I designed the behavioral hardware, control software (BLITZ, C++), and analysis pipelines in Python and MATLAB for operant learning experiments. The same approach now goes into closed-loop hardware, real-time decoders, and signal processing for cardiovascular control.