Biography:
Abstract:
The ketamine-treated sample included 191 unrelated subjects with major depressive disorder (MDD) or bipolar disorder (BD). Changes in depression rating scale score at Day 1 (24 hours post-treatment) were considered the primary outcome, as assessed via the Montgomery-Asberg Depression Rating Scale (MADRS) or the 17-item Hamilton Depression Rating Scale (HAM-D) Ketamine is an antagonist of the glutamate NMDA receptor. Ketamine is thought to work by blocking NMDA receptors on inhibitory GABA-containing interneurons, ultimately promoting glutamate release. We conducted a GWAS analysis, using imputed genotype data. Polygenic risk score analysis was conducted (Ketamine and Scopolamine), below are our preliminary results.
The ketamine-treated sample included 157 unrelated European subjects with major MDD or bipolar disorder (BD). The scopolamine-treated sample comprised 37 unrelated European subjects diagnosed with either MDD or BD who had a current Major Depressive Episode (MDE), and had failed at least two adequate treatment trials for depression. Change in Montgomery–Asberg Depression Rating Scale (MADRS) or the 17-item Hamilton Depression Rating Scale (HAM-D) scale scores at day 1 (24h post-treatment) was considered the primary outcome. Here, we conduct a pilot GWAS analysis to identify potential markers of ketamine response and dissociative side effects. Polygenic risk score analysis of SNPs ranked by the strength of their association with ketamine response was then calculated in order to assess whether common genetic markers from the ketamine study could predict response to scopolamine. Findings require replication in larger samples in light of low power of analyses of these small samples. Nevertheless, our data indicate a promising illustration of our future potential to identify genetic variants underlying rapid treatment response in mood disorders.