Regional cortical thinning of the orbitofrontal cortex in medication-naïve female patients with major depressive disorder is not associated with MAOA-uVNTR polymorphism.

BACKGROUND

Orbitofrontal cortex alterations have been suggested to underlie the impaired mood regulation in depression. -uVNTR (monoamine oxidase A-upstream variable number of tandem repeats) polymorphism has been reported to be associated with major depressive disorder by various studies. The influence of -uVNTR genotype on function and structure of the orbitofrontal cortex has previously been reported. In this study, we investigated the difference in orbitofrontal cortex thickness between medication-naïve female patients with major depressive disorder and healthy controls, and the influence of -uVNTR genotype on orbitofrontal cortex thickness in depression.

METHODS

Thirty-one patients with major depressive disorder and 43 healthy controls were included. All participants were subjected to T1-weighted structural magnetic resonance imaging and genotyped for -uVNTR polymorphism. An automated procedure of FreeSurfer was used to analyze difference in orbitofrontal cortex thickness.

RESULTS

Patients showed a significantly thinner left orbitofrontal cortex ( = 7.941,  = 0.006) and right orbitofrontal cortex ( = 17.447,  < 0.001). For the orbitofrontal cortex sub-region analysis, patients showed a significantly thinner left medial orbitofrontal cortex ( = 8.117,  = 0.006), right medial orbitofrontal cortex ( = 21.795,  < 0.001) and right lateral orbitofrontal cortex ( = 9.932,  = 0.002) compared to healthy controls. No significant interaction of diagnosis and -uVNTR genotype on orbitofrontal cortex thickness was revealed.

CONCLUSIONS

Our results suggest that structural alterations of the orbitofrontal cortex may be associated with the pathophysiology of major depressive disorder. Future studies with larger sample sizes are needed to detect a possible association between -uVNTR genotype and orbitofrontal cortex thickness in depression.