Chronic pain and headache disorders are two leading causes of disability world-wide. Improving treatments for these conditions is a major focus of my lab as well as my clinical practice as a neurologist. The experience of pain begins with specialized peripheral sensory neurons (nociceptors) whose cell bodies reside in dorsal root ganglia at each spinal level or in the trigeminal ganglia at the skull base. Persistent hyperexcitability of nociceptors is thought to underlie many types of chronic pain, but major gaps remain in our understanding of this process. Our group studies the molecular mechanisms underlying nociceptor sensitization with a special interest in headache disorders. Our long-term goal is to identify molecular features that are unique to nociceptors and to leverage this knowledge to develop novel, nociceptor-specific pain therapeutics. Toward this goal, we built single-cell gene expression atlases of both mouse pain models and human nociceptors and are using this information to control nociceptor activity through both genetic loss of function studies in mice and the development of nociceptor-specific viral vectors.

To address these questions, our group uses molecular tools such as single-cell genomics, gene editing, advanced imaging, mouse models, and post-mortem human tissue. We work closely with headache and pain neurology and pathology at the Brigham and Women’s Hospital and Massachusetts General Hospital to accelerate clinical translation of our research.