"Every stress leaves an indelible scar, and the organism pays for its survival after a stressful situation by becoming a little older."
To elucidate the molecular and, in particular, epigenetic underpinnings of stress-related somatic and behavioral conditions
To determine how lasting epigenetic changes result from stressful experiences, accrue throughout life, and contribute to diseases of the aging
To identify novel epigenetic and molecular targets that will enhance our ability to predict, prevent, and treat stress-related conditions
To foster an interdisciplinary, diverse, and creative environment that offers strong mentorship and promotes scientific growth
Psychosocial stress is ubiquitous in modern societies and, especially when chronic or excessive, can have detrimental effects on our bodies. However, each of us will respond to stressful experiences in different ways, for better or for worse. What determines these different responses and outcomes as life progresses? And how exactly does stress “get under the skin"? Among plausible mechanisms, epigenetic changes can regulate genomic function without altering the genetic code. Because these changes can result from environmental exposures, the epigenome acts as a molecular interface that fine-tunes gene and cell function in response to life experiences. We examine how lasting epigenomic patterns result from stressful experiences and shape health or disease trajectories as age advances. To this end, our lab employs a translational approach that combines large-scale analyses in human cohorts with mechanistic investigations in experimental models. We use both bionformatics and wet lab tools. Our passion is to maintain an interdisciplinary, fun environment that promotes creative team work, offers strong mentorship, and fosters scientific growth.