BHI Plenary Seminar (Hybrid): Scott J. Russo, PhD (Icahn School of Medicine at Mount Sinai)

“Neuroimmune Mechanisms of Depression”

Speaker: Scott J. Russo
Leon Levy Director of the Brain-Body Research Institute
Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai

Date and Time: Thursday, Oct 1, 2026, 12 Noon (ET)

Zoom: https://rutgers.zoom.us/j/93226447395?pwd=Rb5AbsEVw5PPkdDC99GKpVOKjJQQqH.1

Meeting ID: 932 2644 7395  |  Passcode: 100126

Location: Staged Research Building (SRB), Room 127
661 Hoes Lane West, Piscataway, NJ

Abstract: Stress-related neuropsychiatric disorders such as major depressive disorder (MDD) and post-traumatic stress disorder (PTSD) have an increasingly high worldwide prevalence and exact tremendous individual burden. While there are some effective treatments for stress disorders, more than a third of affected individuals do not achieve full remission by available antidepressant medications or established psychotherapeutic treatments. One of the most important risk factors for these stress disorders is exposure to chronic psychosocial stress. Therefore, elucidating the pathophysiological mechanisms underlying the effects of psychosocial stress is crucial to advancing our understanding of disorders like MDD and PTSD and ultimately to develop treatment options and prevention strategies. Interactions between the central nervous system (CNS) and other organ systems, including the immune system, are tightly regulated. Psychosocial stress can profoundly impact this bi-directional communication, with disruptions in the neuroimmune axis increasingly recognized as an important factor in the pathogenesis of stress disorders. Chronic stress activates the innate immune system resulting in mobilization of peripheral myeloid cells (i.e., monocytes) and the production of pro-inflammatory cytokines, such as interleukin-6 (IL-6). In humans, it is well established that a subset of patients with stress-related neuropsychiatric disorders display a state of chronic low-grade inflammation, characterized by increased circulating pro-inflammatory cytokines and leukocytosis. The most enduring immune change observed in stress disorder subjects and in mouse chronic stress models is monocytosis, an increase in production and egress of monocytes from bone marrow stores. Interestingly, monocyte levels correlate strongly with quantitative measures of stress suggesting that monocytes might be dynamically regulated. Indeed, our recent work identified a population of stress-responsive neurons in the brain that project to and innervate the bone marrow to control monocytosis. Activation of this circuit by stress increases circulating levels of monocytes and trafficking to target tissues. In addition, stress disrupts the endothelial BBB allowing greater entry of circulating proteins directly into brain reward regions like the NAc. While these findings have provided important insights into the pathophysiology of stress and depression, we still know little about the mechanisms by which these stress-induced peripheral immune changes can affect neuronal function and ultimately behavior. In this talk, I will discuss recent data in both mice and humans to support a model in which peripheral immune cells interface with the brain at the neurovascular unit to control brain circuit function and behaviors relevant to depression and anxiety.

Hosted by Yong Kim, PhD (Neurosurgery/RWJMS)

Learn more about the BHI Plenary Seminar Series