Atrophy of bilateral nucleus accumbens in melancholic depression

无血性 伏隔核 海马体 神经科学 海马结构 萧条(经济学) 扁桃形结构 心理学 病态的 萎缩 医学 重性抑郁障碍 内科学 中枢神经系统 多巴胺 经济 宏观经济学
作者
Zhaosong Chu,Lijin Yuan,Mengxin He,Yuqi Cheng,Yi Lu,Xiufeng Xu,Zonglin Shen
出处
期刊:Neuroreport [Lippincott Williams & Wilkins]
卷期号:34 (10): 493-500 被引量:8
标识
DOI:10.1097/wnr.0000000000001915
摘要

Evidence from previous literature suggests that the nucleus accumbens (NAc), hippocampus, and amygdala play critical roles in the reward circuit. Meanwhile, it was also suggested that abnormalities in the reward circuit might be closely associated with the symptom of anhedonia of depression. However, few studies have investigated the structural alterations of the NAc, hippocampus, and amygdala in depression with anhedonia as the main clinical manifestation. Thus, the current study aimed to explore the structural changes of the subcortical regions among melancholic depression (MD) patients, especially in the NAc, hippocampus, and amygdala, to provide a theoretical basis for understanding the pathological mechanisms of MD. Seventy-two MD patients, 74 nonmelancholic depression (NMD) patients, and 81 healthy controls (HCs) matched for sex, age, and years of education were included in the study. All participants underwent T1-weighted MRI scans. Subcortical structure segmentation was performed using the FreeSurfer software. MD and NMD patients had reduced left hippocampal volume compared with HCs. Meanwhile, only MD patients had reduced bilateral NAc volumes. Moreover, correlation analyses showed correlations between left NAc volume and late insomnia and lassitude in MD patients. The reduced hippocampal volume may be related to the pathogenesis of major depressive disorder (MDD), and the reduced volume of the NAc may be the unique neural mechanism of MD. The findings of the current study suggest that future studies should investigate the different pathogenic mechanisms of different subtypes of MDD further to contribute to the development of individualized diagnostic and treatment protocols.
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