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

Eunsoo Won; Sunyoung Choi; June Kang; Min Soo Lee; Byung Joo Ham

doi:10.1186/s12991-016-0116-0

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

Eunsoo Won, Sunyoung Choi, June Kang, Min Soo Lee, Byung Joo Ham

Research output: Contribution to journal › Article › peer-review

8 Citations (Scopus)

Abstract

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.

Original language	English
Article number	26
Journal	Annals of General Psychiatry
Volume	15
Issue number	1
DOIs	https://doi.org/10.1186/s12991-016-0116-0
Publication status	Published - 2016 Oct 12

Bibliographical note

Funding Information:
This work was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Educa‑ tion, 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.

Publisher Copyright:
© 2016 The Author(s).

Keywords

Major depressive disorder
Monoamine oxidase A-upstream variable number of tandem repeats
Orbitofrontal cortex thickness

ASJC Scopus subject areas

Psychiatry and Mental health

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1186/s12991-016-0116-0

Cite this

@article{bbb0858c9b9643a68cf2617d10160268,

title = "Regional cortical thinning of the orbitofrontal cortex in medication-na{\"i}ve female patients with major depressive disorder is not associated with MAOA-uVNTR polymorphism",

abstract = "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-na{\"i}ve 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.",

keywords = "Major depressive disorder, Monoamine oxidase A-upstream variable number of tandem repeats, Orbitofrontal cortex thickness",

author = "Eunsoo Won and Sunyoung Choi and June Kang and Lee, {Min Soo} and Ham, {Byung Joo}",

note = "Funding Information: This work was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Educa‑ tion, 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. Publisher Copyright: {\textcopyright} 2016 The Author(s).",

year = "2016",

month = oct,

day = "12",

doi = "10.1186/s12991-016-0116-0",

language = "English",

volume = "15",

journal = "Annals of General Psychiatry",

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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: This work was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Educa‑ tion, 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. Publisher Copyright: © 2016 The Author(s).

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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SN - 1744-859X

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

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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