Specialties

While driven by a passion for developing innovative approaches to understand and treat psychosis risk states, I remain deeply connected with my patients and their families. I am also dedicated to educating the next generation of behavioral health professionals and am recognized as an esteemed lecturer on medications for treating psychosis risk and comorbidities. What sets me apart in my approach to patient care is my integration of holistic and compassionate personalized care with cutting edge neuroscience. I appreciate the significance of developmental and neurobiological principles while also acknowledging the impact of environmental, cultural, and psychological factors on distressing symptoms and experiences. This comprehensive approach ensures that each patient receives tailored care that addresses their unique needs. One of my main goals has been to advance understanding, investigation, and treatment of psychiatric disorders until they are eliminated as a cause of human suffering. To that end, I have spent many years studying the molecular mechanisms underlying cognitive dysfunction in schizophrenia, with an emphasis on understanding the cell and circuit specific developmental trajectories of these key molecular components. The underlying motivation for studying the development and dysfunction of cognitive control in schizophrenia is to improve patients’ lives by identifying biologically-informed innovative approaches to treat cognitive dysfunction in schizophrenia and by ideally preventing or delaying the premorbid developmental lag in cognitive control and the onset of psychosis in people with schizophrenia. Together, we must alleviate our patients’ suffering by reducing the burden of and eliminating these psychiatric disorders.  My interest in TMS neuromodulation grew from years of research into molecular and cellular components of neural circuits that are altered in schizophrenia postmortem human tissue. Studying subtypes of glutamate and GABA neurons taught me the importance of specificity and precision when investigating a complex syndrome like schizophrenia. My work also led to the speculation that increasing activity in the prefrontal cortex and decreasing activity in the visual cortex might normalize changes in glutamate and GABA neurotransmission underlying cognitive dysfunction in schizophrenia, an idea that could potentially be tested with TMS.