TY - JOUR
T1 - Regional cortical thinning of the orbitofrontal cortex in medication-naïve female patients with major depressive disorder is not associated with MAOA-uVNTR polymorphism
AU - Won, Eunsoo
AU - Choi, Sunyoung
AU - Kang, June
AU - Lee, Min Soo
AU - Ham, Byung Joo
N1 - Funding Information:
Not applicable. This work was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (NRF-2011-0023272) and the Korean Health Technology R&D Project, Ministry of Health and Welfare, Republic of Korea (HI12C0003). The funder had no role in the design of the study and collection, analysis, and interpretation of data and in writing the manuscript.
PY - 2016/10/12
Y1 - 2016/10/12
N2 - Background: Orbitofrontal cortex alterations have been suggested to underlie the impaired mood regulation in depression. MAOA-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 MAOA-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 MAOA-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 MAOA-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 (F (1,71) = 7.941, p = 0.006) and right orbitofrontal cortex (F (1,71) = 17.447, p < 0.001). For the orbitofrontal cortex sub-region analysis, patients showed a significantly thinner left medial orbitofrontal cortex (F (1,71) = 8.117, p = 0.006), right medial orbitofrontal cortex (F (1,71) = 21.795, p < 0.001) and right lateral orbitofrontal cortex (F (1,71) = 9.932, p = 0.002) compared to healthy controls. No significant interaction of diagnosis and MAOA-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 MAOA-uVNTR genotype and orbitofrontal cortex thickness in depression.
AB - Background: Orbitofrontal cortex alterations have been suggested to underlie the impaired mood regulation in depression. MAOA-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 MAOA-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 MAOA-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 MAOA-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 (F (1,71) = 7.941, p = 0.006) and right orbitofrontal cortex (F (1,71) = 17.447, p < 0.001). For the orbitofrontal cortex sub-region analysis, patients showed a significantly thinner left medial orbitofrontal cortex (F (1,71) = 8.117, p = 0.006), right medial orbitofrontal cortex (F (1,71) = 21.795, p < 0.001) and right lateral orbitofrontal cortex (F (1,71) = 9.932, p = 0.002) compared to healthy controls. No significant interaction of diagnosis and MAOA-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 MAOA-uVNTR genotype and orbitofrontal cortex thickness in depression.
KW - Major depressive disorder
KW - Monoamine oxidase A-upstream variable number of tandem repeats
KW - Orbitofrontal cortex thickness
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U2 - 10.1186/s12991-016-0116-0
DO - 10.1186/s12991-016-0116-0
M3 - Article
AN - SCOPUS:84991214892
VL - 15
JO - Annals of General Psychiatry
JF - Annals of General Psychiatry
SN - 1744-859X
IS - 1
M1 - 26
ER -
