Study Report
Reference
| Citation | Friedel, 2009 PubMed |
| Full Info | Friedel, E., Schlagenhauf, F., Sterzer, P., Park, S.Q., Bermpohl, F., Strohle, A., Stoy, M., Puls, I., Hagele, C., Wrase, J. et al. (2009) 5-HTT genotype effect on prefrontal-amygdala coupling differs between major depression and controls. Psychopharmacology (Berl), 205, 261-271.
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Study
| Hypothesis or Background |
In major depression, prefrontal regulation of limbic brain areas may be a key mechanism that is impaired during the processing of affective information. This prefrontal-limbic interaction has been shown to be modulated by serotonin (5-HTT) genotype, indicating a higher risk for major depressive disorder (MDD) with increasing number of 5-HTT low-expression alleles.
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| Sample Information | 21 unmedicated patients with MDD compared to 21 matched healthy controls |
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| Method Detail | Functional magnetic resonance imaging was used to assess neural response to uncued unpleasant affective pictures in 21 unmedicated patients with MDD compared to 21 matched healthy controls, taking into account genetic influences of the 5-HTT (SCL6A4) high- and low-expression genotype. |
| Method Keywords | functional magnetic resonance imaging (fMRI); genotyping |
| Result | Healthy controls displayed greater prefrontal activation (BA10) to uncued negative pictures compared to patients with MDD. While in healthy controls prefrontal (BA10) activation and BA10-amygdala coupling increased with the number of 5-HTT low-expression risk alleles, this effect was abolished, and even reversed, in patients with MDD. In MDD, connectivity decreased with severity of depressive symptoms (HAMD total score). |
| Conclusions | These findings suggest that increased medial prefrontal (BA10) activation and BA10-amygdala connectivity may counteract the risk for MDD in healthy carriers of 5-HTT low-expression alleles, while this protective factor might be lost in patients who actually suffer from MDD. Prefrontal-limbic regulation in risk populations could be a target of early interventions and should be the focus of further research. |
Relationships reported by
Friedel, 2009
| Component A Approved Name (Name in Paper) |
Component A Type |
Component B Approved Name (Name in Paper) |
Component B Type |
Statistical Result |
Relationship Description |
Result Category (Positive/Negative)) |
|
Prefrontal cortex (prefrontal cortex)
|
brain morphology and function |
SLC6A4 (5-HTT) |
gene |
|
In healthy controls prefrontal (BA10) activation and BA10-amygdala coupling increased with the number of 5-HTT low-expression risk alleles, this effect was abolished, and even reversed, in patients with MDD. |
Positive
|
|
Amygdala (amygdala)
|
brain morphology and function |
SLC6A4 (5-HTT) |
gene |
|
In healthy controls prefrontal (BA10) activation and BA10-amygdala coupling increased with the number of 5-HTT low-expression risk alleles, this effect was abolished, and even reversed, in patients with MDD. |
Positive
|
|
MDD
|
syndrome |
Prefrontal cortex (prefrontal cortex) |
brain morphology and function |
|
In healthy controls prefrontal (BA10) activation and BA10-amygdala coupling increased with the number of 5-HTT low-expression risk alleles, this effect was abolished, and even reversed, in patients with MDD. |
Positive
|
|
MDD
|
syndrome |
Amygdala (amygdala) |
brain morphology and function |
|
In healthy controls prefrontal (BA10) activation and BA10-amygdala coupling increased with the number of 5-HTT low-expression risk alleles, this effect was abolished, and even reversed, in patients with MDD. |
Positive
|
