Ignite Creation Date:
2024-10-26 @ 3:42 PM
Last Modification Date:
2024-10-26 @ 3:42 PM
Study NCT ID:
NCT06630065
Status:
RECRUITING
Last Update Posted:
None
First Post:
2024-09-26
Brief Title:
Study of the Neural Circuits Underlying the Negative Emotional Bias of Depressive Disorders and Their Response to Ketamine
Sponsor:
None
Organization:
None
Study Overview
Official Title:
Translational Study of the Neural Circuits Underlying the Negative Emotional Bias of Depressive Disorders and Their Response to Ketamine
Status:
RECRUITING
Status Verified Date:
2024-10
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
No
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
EMOKET
Brief Summary:
Major depressive disorder is the leading cause of disability worldwide affecting up to 300 million people each year and one in five people will experience depression at least once in their lives Emotional bias is an essential component of characterized depressive episodes leading depressed patients to attribute a more negative valence to emotional stimuli
On the basis of recent and robust neuroscientific data revisiting the role of the cerebral amygdala as an essential essential structure for encoding the negative and positive valences and of emotional stimuli the team has shown in mice that a depressive phenotype induced by a chronic administration of corticosterone a well-known model of depression is associated with a change in hedonic value allocation ie pleasant odors become less pleasant and aversive odors become even more unpleasant mimicking what happens in humans identical data in humans
It assumes that
1 There is a negative emotional bias in depressed patients compared with control subjects evidenced by the assignment of more negative valences when viewing images
2 In depressed subjects compared with controls subjects there is greater activation of the basolateral amygdalaventral hippocampus pathway the level of imaging resolution of imaging does not allow to study the basolateral amygdalacentral amygdala pathway in humans and less of the basolateral amygdalanucleus accumbens pathway
3 In depressed subjects improvement in negative emotional bias correlated with a good response after after 4 weeks of treatment with esketamine Spravato measured by a 50 reduction in the Montgomery-Åsberg Depression Rating Scale
4 In depressed patients early improvement of emotional bias after a single administration is predictive of response to treatment at 4 weeks
5 In depressed patients with a good response to a single 4-weeks course of esketamine Spravato a normalization of activation of basolateral amygdalaventral hippocampus and basolateral amygdalanucleus accumbens pathways is observed
6 Depressed subjects have different immunoinflammatory and RNA editing patterns different from control subjects
7 In depressed patients clinical improvement correlates with normalization of patients inflammatory profile and certain mRNA editing
8 Some clinical features of major depressive disorder are associated with greater negative emotional bias significant
On the basis of recent and robust neuroscientific data revisiting the role of the cerebral amygdala as an essential essential structure for encoding the negative and positive valences and of emotional stimuli the team has shown in mice that a depressive phenotype induced by a chronic administration of corticosterone a well-known model of depression is associated with a change in hedonic value allocation ie pleasant odors become less pleasant and aversive odors become even more unpleasant mimicking what happens in humans identical data in humans
It assumes that
1 There is a negative emotional bias in depressed patients compared with control subjects evidenced by the assignment of more negative valences when viewing images
2 In depressed subjects compared with controls subjects there is greater activation of the basolateral amygdalaventral hippocampus pathway the level of imaging resolution of imaging does not allow to study the basolateral amygdalacentral amygdala pathway in humans and less of the basolateral amygdalanucleus accumbens pathway
3 In depressed subjects improvement in negative emotional bias correlated with a good response after after 4 weeks of treatment with esketamine Spravato measured by a 50 reduction in the Montgomery-Åsberg Depression Rating Scale
4 In depressed patients early improvement of emotional bias after a single administration is predictive of response to treatment at 4 weeks
5 In depressed patients with a good response to a single 4-weeks course of esketamine Spravato a normalization of activation of basolateral amygdalaventral hippocampus and basolateral amygdalanucleus accumbens pathways is observed
6 Depressed subjects have different immunoinflammatory and RNA editing patterns different from control subjects
7 In depressed patients clinical improvement correlates with normalization of patients inflammatory profile and certain mRNA editing
8 Some clinical features of major depressive disorder are associated with greater negative emotional bias significant
Detailed Description:
None
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None