“Tracking Dynamic Immune Activation and Invasion in Neurological Diseases Using PET”
For inquiries contact Michelle Hoelscher
Brief Bio: Dr. James is an Assistant Professor in the Departments of Radiology and Neurology, within the Molecular Imaging Program at Stanford (MIPS). She received her BS in pharmacology and medicinal chemistry at the University of Sydney, where she also earned her PhD in radiochemistry and was awarded the University Medal. Dr. James’s research is focused on developing novel molecular imaging agents to improve the way we diagnose, treat, and understand devastating neurological diseases such as Alzheimer’s and Multiple Sclerosis. As part of her work, Dr. James has multiple patented PET radiotracers for imaging brain diseases, four of which are currently being used in clinical studies at Stanford and/or around the world. She recently cofounded a company called Willow Neuroscience which is focused on developing immunomodulatory therapeutics and novel PET diagnostics for neurodegenerative diseases.
Abstract: Neuroinflammation is a key pathological feature of many central nervous system (CNS) diseases. Although extensive work in preclinical rodent models demonstrate a significant role for both the innate and adaptive immune response in the initiation and progression of neurological diseases, our understanding of these responses and their contribution to human disease remains very limited. Additionally, both beneficial and toxic inflammatory processes are associated with progression and remission of neurological disease, and the spatiotemporal course of these complex responses remain a mystery especially in the clinical setting. Molecular imaging using positron emission tomography (PET) has enormous potential as a translatable technique to enhance our understanding of neuroinflammation in CNS diseases. Our experience with developing new PET radioligands for visualizing the neuroinflammatory component of Alzheimer’s disease, multiple sclerosis, and stroke will be described. I will provide examples regarding our work on designing radioligands for the translator protein 18 kDa (TSPO), triggering receptor expressed on myeloid cells 1 (TREM1), and two B lymphocyte surface antigens. Specifically, the in vivo role, spatiotemporal dynamics, peripheral contribution and different functional phenotypes of innate and adaptive immune cells throughout the progression of CNS diseases will be shown. Moreover, I will describe how we are starting to apply these tools to track disease progression, guide therapeutic selection for individual patients, and serve as surrogate endpoints in clinical trials.