Division of Experimental and Molecular Psychiatry, Department of Psychiatry, Psychotherapy and Preventive Medicine, LWL University Hospital, Ruhr-University Bochum, Germany.
School of Medicine, University of St Andrews, United Kingdom.
J Affect Disord. 2021 Mar 1;282:91-97. doi: 10.1016/j.jad.2020.12.056. Epub 2020 Dec 21.
Alterations in the hippocampus and prefrontal cortex (PFC) have frequently been reported in depressed patients. These parameters might prove to be a consistent finding in depression. In addition, peripheral DNA methylation of the MORC1 gene promoter showed stable associations with depression across independent samples. However, the question arises whether MORC1, supposedly acting as transcription factor, might also be involved in neurobiological alterations accompanying depression. This study further analyses the role of MORC1 in depression by investigating a potential correlation between peripheral MORC1 DNA methylation and neuronal structural properties previously associated with depression in humans.
Beck Depression Inventory (BDI) was assessed in 52 healthy participants. DNA was extracted from buccal cells and MORC1 methylation correlated with micro- and macrostructural properties derived from magnetic resonance imaging (MRI) and neurite orientation dispersion and density imaging (NODDI) in the hippocampus and medial prefrontal cortex (mPFC).
MORC1 methylation was associated with volume reduction and neurite orientation dispersion and density markers in the hippocampus and mPFC. BDI was positively associated with neurite orientation dispersion and density markers in the hippocampus.
The study was conducted in a small sample of healthy participants with subclinical depressive symptoms. Peripheral tissue was analyzed.
We found significant negative associations between peripheral MORC1 methylation and macro- and microstructural markers in the hippocampus and mPFC. Thus, MORC1 might be involved in neurobiological properties. Studies investigating neuronal methylation patterns of MORC1 are needed to support this hypothesis.
抑郁症患者的海马体和前额叶皮层(PFC)经常发生变化。这些参数可能在抑郁症中是一个一致的发现。此外,MORC1 基因启动子的外周 DNA 甲基化与抑郁症在独立样本中表现出稳定的关联。然而,问题是,MORC1 作为转录因子,是否也可能参与伴随抑郁症的神经生物学改变。本研究通过研究与人类抑郁症相关的外周 MORC1 DNA 甲基化与先前与抑郁症相关的神经元结构特性之间的潜在相关性,进一步分析了 MORC1 在抑郁症中的作用。
在 52 名健康参与者中评估贝克抑郁量表(BDI)。从颊细胞中提取 DNA,并将 MORC1 甲基化与从磁共振成像(MRI)和神经丝取向分散和密度成像(NODDI)获得的海马体和内侧前额叶皮层(mPFC)中的微观和宏观结构特性相关联。
MORC1 甲基化与海马体和 mPFC 中的体积减少和神经丝取向分散和密度标记物相关。BDI 与海马体中的神经丝取向分散和密度标记物呈正相关。
该研究在具有亚临床抑郁症状的健康小样本参与者中进行。分析了外周组织。
我们发现外周 MORC1 甲基化与海马体和 mPFC 中的宏观和微观结构标记物之间存在显著的负相关。因此,MORC1 可能参与神经生物学特性。需要研究神经元 MORC1 甲基化模式的研究来支持这一假设。