Research

Our research lies at the intersection between neurodegeneration and behavioral states. We take a systems approach, trying to understand biology from the molecular, cellular, and organismal level.

Research Themes:

Cortical Encoding of Somatosensation and Pain-related Behavioral States

The extraordinary breadth and encoding capacity of our somatosensory and pain system relies on a network of interconnected, surprisingly still undefined, neural circuits. Sensation detection originates in the peripheral nervous system and is transmitted to the central nervous system for stimulus perception and integration with deeper cognitive processes such as emotion and memory. Anatomical connectivity has established the cerebral cortex as the penultimate site of information processing and contains two distinct somatosensory processing regions termed the primary and secondary somatosensory cortices (S1 and S2), respectively. The prevailing hypothesis is that these two structures work together to produce an accurate perception of the stimulus being sensed. Rather, these two distinct regions appear to encode different modalities and intensities of sensory information, yet it is still unknown how information is processed in these regions at a cellular level. Using a set of newly developed methodologies and experimental animal models, combined with human neuromodulation studies we ask:

• How is sensation represented in the cortex and how does this change during pain?
• Can we use neuromodulatory therapeutics to treat chronic pain?

Molecular Mechanisms Driving Peripheral Neurodegeneration and Regeneration

Axons are the physical wires that connect our nervous system together. However, their structures are delicate, sensitive to their cellular environment, become compromised with age, and have limited capacity for regeneration. When they degenerate in the peripheral nervous system, it results in a devastating disease called neuropathy that causes immense pain. This is becoming an increasingly prevalent disease, particularly in those with diabetes and in the aging population. In fact, it accounts for the highest number of patient visits in out-patient Neurology offices. Unfortunately, there are little therapeutic options to treat the pain and none to prevent or delay the degeneration from occurring. We aim to ask the following big questions:

• What are the genetic and dietary risk factors for axon degeneration?
• Can we develop therapeutics to delay, prevent, or restore the health of axons?
• How can we quickly enable a successful regenerative response?

This video depicts our imaging of calcium handling in single axons over time and during degeneration/regeneration.