Paul Jenkins, Ph.D.

Assistant Professor of Pharmacology
Assistant Professor of Psychiatry
University of Michigan Medical School

“Defining how genetic changes alter brain circuitry and activity will provide a critical framework for understanding why people experience mood disorders. Collaboration with the Prechter Program gives us the power to enhance our understanding of the disease from multiple angles."

-Paul Jenkins, Ph.D.

Biography

Dr. Jenkins received his B.S. degree from the University of Michigan, and received a Ph.D. in Pharmacology from the University of Michigan. He continued his training as a postdoctoral fellow at the Howard Hughes Medical Institute at Duke University.

Dr. Jenkins is an Assistant Professor of Pharmacology and Psychiatry at the University of Michigan Medical School. During his postdoctoral work, Dr. Jenkins and colleagues uncovered a new role for a giant splice variant of ankyrin-G (product of the ANK3 gene) in the formation of critical circuits that are responsible for generation of gamma oscillations, critical brain rhythms that are often disrupted in bipolar patients. Dr. Jenkins’ current research is focused on understanding the cellular and molecular underpinnings of complex psychiatric diseases like bipolar disorder. The goal of his research is to identify the signaling pathways and circuits that are altered in disease in order to find better therapies.

As a researcher within the Heinz C. Prechter Bipolar Research Program, Dr. Jenkins is interested in the effects of human variants in the ANK3 gene on neuronal cell biology and cortical circuitry. To address this goal, his laboratory utilizes cellular and molecular biology, animal models, microscopy, electrophysiology, as well as human neurons derived from patients participating in the Prechter Longitudinal Study of Bipolar Disorder. The detailed clinical and biological data and patient samples gathered from the research volunteers are an extremely valuable source of information that can help us shed light on the mechanisms of disease and hopefully design better, more effective therapies for the treatment of bipolar disorder.