My research takes a developmental approach to the study of early signs of severe mental illness, especially psychosis development. Specifically, in my research I investigate signs of psychosis risk that contribute to symptom progression and illness onset. My research ultimately aims to identify factors that will be the most malleable targets for intervention.


This perspective on psychosis risk has emerged from two themes; 1) the role of developmental processes in the pathogenesis of psychosis, and 2) the importance of the adolescent period as a critical stage for studying these developmental changes. Abnormal neurodevelopmental processes (e.g., changes in hormones) in adolescence may trigger the expression of latent vulnerability to psychosis. Accumulating evidence demonstrates that adolescence is the modal stage for the onset of the psychosis clinical risk syndrome, which is characterized by subclinical symptoms and functional decline in academic and vocational activities.


Consistent with a neurodevelopmental perspective of mental illness in adolescence, I have become particularly interested in the role of hormones in the development of psychosis (Trotman et al., 2013). It is possible that changes in hormones trigger the expression of latent aberrant genetic vulnerabilities. Alternatively, it may be that neurohormonal changes that control normal neuromaturational processes during adolescence interact with preexisting vulnerabilities. Although not much is known about the relationship between gonadal hormones and the development of psychosis, the well-established sex difference in age at onset and course of illness in psychosis suggests a pivotal role for these hormones.


Adolescence/young adulthood is the modal period for the onset of prodromal and psychotic symptoms. This may stem from the increased stress sensitivity during this time, which has been a central factor in neurodevelopmental models of psychosis. In fact, increased stress sensitivity at baseline differentiates individuals with clinical high risk symptoms who remit compared to those who develop psychosis after two years (Trotman et al., 2014). These factors heighten the need to better understand the nature of hormonal processes during adolescence, particularly the association between Hypothalamic-Pituitary-Gonadal (HPG) and Hypothalamic-Pituitary Adrenal (HPA) activity. Animal studies show evidence of a bidirectional relationship. Although many interactions among the HPA and HPG axes remain to be delineated in the literature; these systems have wide ranging applicability for a variety of psychiatric conditions with typical onset in adolescence and sex differences in phenomenology.


I am interested in working with Mercer undergraduates who are fascinated by important questions at the intersection of clinical neuroscience and developmental psychopathology. If you are a Mercer undergraduate and interested in learning about various aspects of clinical research, please complete the online form to apply to my research group.