Dr. Etienne L. Sibille is Chair of the Campbell Family Mental Health Research Institute and Senior Scientist at the Centre for Addiction and Mental Health. He is also a Professor in the Department of Psychiatry and the Department of Pharmacology and Toxicology at the University of Toronto.
Dr. Sibille’s research goals have consistently focused on translational research aimed at identifying the cellular and molecular bases of depression, specifically of the mood, affect and cognitive components of the illness. His laboratory studies encompass parallel investigations in postmortem brains of depressed and control subjects, and in preclinical genetic and environmental models, with the aims of characterizing the primary pathology of depression and assessing causal links between identified molecular changes or candidate neurotransmitter systems and mood regulation. Current projects include translating human postmortem findings on the role of the GABA microcircuitry in mood regulation, and specifically of reduced somatostatin-positive dendritic targeting interneuron function.
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This session seems primarily a cheerleading effort with very few,, if any specifics. Dr. Sibille’s stance is based on what the future may hold, as he notes recent technological advances, but fails utterly to describe any significant clinical advances secondary to those developments. We have been promising breakthroughs for decades, but, despite the technical advances, we are still treating depression based on medications developed 50 years ago. Not a single antidepressant has been developed on the basis of genetic findings, or neuroimaging discoveries.
Thank you for taking the time and the trouble to comment. We share your frustration over the lack of progress in developing pathophysiologically based treatements so far. We think, though, that Dr. Sibille is right to be hopeful about the near future. The RDoC has allowed groups to study the processes underlying mood dysregulation separate from heterogeneous clinical diagnoses and this is leading to grant submissions targeting specific neural pathways underlying these dysregulations. As is happening in autism using genetic markers, subsets of patients with “major depressive disorder” are being identified as resistant to traditional antidepressants on the basis of inflammatory biomarkers, (https://www.ncbi.nlm.nih.gov/pubmed/26169573) and another subset of patients refractory to standard treatment appear to have cerebral folate deficiency, (https://www.ncbi.nlm.nih.gov/pubmed/27523499). These are new treatment pathways which at the moment help only a few people presenting with depression, but are very real evidence of the shift in evidence for which you seek. Thank you again, Mike, Dave and Melissa on behalf of the NNCI