Yu-Shin Ding, PhD

I have over 25 years of experience in the development and application/evaluation of novel PET ligands for translational research to study various disorders and biochemistry and mechanisms of drug action in living humans using PET, where my role is to bridge the fields of chemistry, biology and medicine. I have served as PI in various drug occupancy studies for phase I and phase II clinical trials for drug research and drug development in collaboration with pharmaceutical companies (Pfizer, GSK, etc.). I currently serve as the PI of several imaging grants studying drug mechanisms, obesity, tau and sleep. Our decades-long studies in humans using a norepinephrine transporter (NET) selective radiotracer ([¹¹C]MRB) (>40 publications) have demonstrated a selective vulnerability of the LC-NE system to aging and stress and to various disorders; e.g., cocaine addiction, ADHD, PTSD, obesity, brown fat, diabetes, and cardiovascular dysfunction. My recent preliminary data reveals, for the first time, that the decline rate of NET, normally associated with aging due to loss in NET availability and cell death, is much faster in blacks starting in their mid-30s, particularly in black males. These results led to the novel molecular insight for the mechanistic characterization of the health disparity in aging and Alzheimer's disease, as the current biomarker classification system (i.e., the ATN model) may not fully account for the racial differences in AD risks. We propose that a faster decline of LC-NE function (decreased NET availability), resulting from chronic stress, occurs in blacks in midlife and at preclinical stages of AD and is responsible for the different disease expression among blacks.