One of the major objectives of the UAB Depression and Suicide Center is to elucidate the neurobiological basis of mood disorders and suicide, not only to increase the understanding of the fundamental mechanisms of these disorders, but also to enable the development of better treatments. The basic and translational research pertaining to mood disorders and suicide are overseen by Dr. Yogesh Dwivedi, who was recruited to the Department of Psychiatry at UAB in 2013 as an internationally reputed researcher in the areas of depression and suicide. Since then, he has continued to make significant strides in the field of depression and suicide research through consistent funding from the National Institute of Mental Health and the American Foundation for Suicide Prevention. Dr. Dwivedi’s research elucidates the molecular and cellular mechanisms associated with mood disorders, stress-related pathology, and suicidal behavior by integrating basic and clinical neuroscience to comprehensively examine the fundamental roles of neurotransmitter receptors, non-coding RNAs, neuroinflammation, cellular signaling, and neural plasticity by utilizing various novel and cutting-edge molecular, cellular, bio-computational, and bio-behavioral tools. The model systems that he uses include human postmortem brain, peripheral blood cells, iPSCs, as well as pharmacological and behavioral rodent models of depression, impulsivity, and PTSD.
Dr. Dwivedi’s innovative studies aim to better grasp the characteristics of depressed individuals, focusing on issues such as early-life adversity, and neurobiological factors, with particular attention to how the environment interacts with the genome to increase the risk for depression and suicidal behavior. His studies of aberrant miRNA expression and how their epigenetic modification can lead to deficits in the coping response to stress, is resulting in the identification of new non-coding RNA-based therapeutic targets. He has initiated a large-scale translational study to investigate the efficacy of acute dose of ketamine as anti-suicidal/antidepressant agent in the patient population, and to examine whether neural-derived exosomal miRNAs can be used to distinguish patients who are responsive or non-responsive to this novel treatment paradigm. Similar approaches are being used to identify peripheral biomarkers for suicidality among depressed patients. His most recent research is focusing on how aberrant expression of non-coding RNAs and epigenetic modifications of coding and non-coding genes mediate childhood maltreatment-induced depression and suicidality during adolescence and adulthood. Another significant area of his research, that m6A methylation may act as a dynamic regulator of gene expression, has tremendous potential for the discovery of unique epitranscriptome-based gene regulation as a mechanism in MDD etiology and for identifying novel targets for therapeutic intervention.