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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.
Won, Eunsoo; Choi, Sunyoung; Kang, June; Lee, Min-Soo; Ham, Byung-Joo.
Afiliação
  • Won E; Department of Psychiatry, Korea University Anam Hospital, Korea University College of Medicine, 73, Inchon-ro, Seongbuk-gu, Seoul, 136-705 Republic of Korea.
  • Choi S; Department of Brain and Cognitive Engineering, Korea University, Seoul, Republic of Korea.
  • Kang J; Department of Biomedical Science, Korea University, Seoul, Republic of Korea.
  • Lee MS; Department of Psychiatry, Korea University Anam Hospital, Korea University College of Medicine, Seoul, Republic of Korea.
  • Ham BJ; Department of Psychiatry, Korea University Anam Hospital, Korea University College of Medicine, 73, Inchon-ro, Seongbuk-gu, Seoul, 136-705 Republic of Korea.
Ann Gen Psychiatry ; 15: 26, 2016.
Article em En | MEDLINE | ID: mdl-27752275
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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Risk_factors_studies Idioma: En Revista: Ann Gen Psychiatry Ano de publicação: 2016 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Risk_factors_studies Idioma: En Revista: Ann Gen Psychiatry Ano de publicação: 2016 Tipo de documento: Article