VBP Research 2026

The central goal of the Glimcher laboratory is to develop and advance interdisciplinary models of human choice that combine insights from neuroscience, psychiatry, economics and psychology. Using methods ranging from interventional clinical trials to brain imaging to computational models of neural calculations, the laboratory seeks to identify the brain-computations responsible for decision-making and to see how these mechanisms go awry in a number of psychiatric disorders. Of particular interest to the lab are disorders where we know decision-making is affected, like Substance Use Disorders, Major Depressive Disorder and Post-traumatic Stress Disorder. In our studies of substance use disorder we have shown that relapses occur just after patients begin to become more risk-tolerant. We have developed clinical interventions based on this signal and are now running a clinical trial in which we are attempting to predict and prevent relapses. In the area of depression, we have recently demonstrated that a key variable in human decision-making, the so-called decisional reference point which won Daniel Kahneman the Nobel Prize in economics, is disordered in patients with depression. We are now using that insight to develop a new highly-reliable test for depression that we hope will guide treatment in new ways. In the area of PTSD we are working to build a better understanding of how treatments restore both healthy behavior and normal decision-making, and to see how closely intertwined are these features. In sum, the laboratory uses a broad range of empirical and theoretical tools in its effort to better understand both how people and animals choose and how to develop diagnostics, treatments, and even social policies thatmaximize the welfare of humans and animals everywhere.he psychiatric origin of AN by testingwhether injections of ABA animals with sub-anesthetic ketamine can ameliorate ABAvulnerability. Our findings are that ketamine doesreduce ABA vulnerability, not only by reducinghunger-evoked hyperactivity but also by increasingcaloric intake. Compared to KG, ketamine’s effect isweaker but longer-lasting. Based on results fromthe metabolic and psychiatric goals, our currentgoal is to examine whether combining KG withketamine reduces ABA vulnerability even more.

Next steps: Results from this study showed that BDNF levels inthe hippocampus are elevated greatly by the ABA-inducing environment, likely due to heightened exercising . However, BDNF level is elevated equallyfor animals fed standard diet or KG. Ketone bodiesare heightened by KG but not by exercise alone orfasting alone or under the ABA-inducing condition ofexercise plus fasting but fed standard diet. In thefuture, we would like to go after the hypothesis thatketone bodies evoke synaptic plasticity to improveresilience against ABA.