Pfizer Canada Professor in Pain Research, and Canada Research Chair (Tier 1) in Human Pain Genetics
My lab investigates the psychological, molecular, cellular, and genetic pathways that mediate both acute and persistent pain states. Our primary goal is to identify the critical elements of human genetic variability contributing to pain sensitivity and pathophysiological pain states that will enable individualized treatments and therapies. Other related research endeavors include molecular hierarchy and evolution of functional SNPs (single-nucleotide polymorphisms), regulation of gene expression underlying molecular pain signaling, testing of surrogate pain animal models for genes influencing human pain, and clustering of neurological and psychological phenotypes that contribute to human persistent pain conditions. Answering these questions requires collaboration with experts in both clinical and basic biological sciences. Such collaborative activities allow my lab to take basic genetic findings all the way from human association studies, through molecular and cellular mechanisms, to animal models, and ultimately to human clinical trials.
Current research projects in my lab include:
- Identifying critical elements of human genetic variability contributing to pain sensitivity and athophysiological pain states through genome-wide approaches.
- Identifying SNP-dependent regulation of gene function underlying variability in human molecular pain signaling.
- Identifying ways to enable individualized treatments and therapies for human pain.
Persistent pain is a part of many common human clinical conditions, yet the current ability to diagnose and manage these conditions is inadequate. Pain perception is one of the most complicated measurable traits, as it is composed of an aggregate of several other measurable phenotypes associated with peripheral and central nervous system dynamics, stress responsiveness, and inflammatory state. It is generally accepted that complex traits, like pain perception, result from the interplay between environmental exposures and multiple genetic variants. However, little is known about the nature of these genetic variants. Because of the established roles of environmental exposures and the commonly held view that pain perception is an unquantifiable