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Mounira Banasr
PhD
Qualification
- PhD in Neuroscience from the University of Sciences of Luminy, France in 2004
Dr. Mounira Banasr received her PhD in Neuroscience from the University of Sciences of Luminy, France in 2004. She went on to complete her post-doctoral fellowship at Yale's Department of Psychiatry, in the laboratory of Ronald Duman, where she became a Junior Scientist in 2008. Dr. Banasr comes to University of Toronto with extensive experience in mechanisms of depression, stress-related illnesses, and novel antidepressants. She contributed seminal work in these fields, including 1) demonstrating in rodent that astroglial dysfunction participate to the expression of depressive-like behaviors and can be targeted for antidepressant treatment, 2) identifying similar synaptic loss and dysfunction in both human depression and chronic stress rodent models and 3) elucidating the cellular and molecular substrates involved in the rapid antidepressant response of ketamine-like drugs. Dr. Banasr uses cutting-edge viral and genetic tools to establish a causal link between region-specific and/or cell-specific changes in target genes or molecules and behavioral outcomes in paradigms relevant to multiple psychiatric disorders including depression. Her research relies on highly translational topics and approaches and combines postmortem studies and chronic stress models to validate the relevance of specific cellular changes in the etiology and for the treatment of major depressive disorder. Her primary interest resides in the investigation of the key molecules, cells and pathways implicated in the expression of the symptoms of depression. Dr. Banasr's work focuses on the most consistent findings from human post-mortem studies in depression, the GABAergic, synaptic and astroglial dysfunctions associated with this disorder, and their involvement in the expression of depressive-like behaviors and cognitive impairment. She anticipates that this approach will provide new therapeutic leads for the development of more selective and efficient drugs for the treatment of depression, specifically that targeting these cellular pathologies is a promising new avenue for the development of antidepressant treatments.