Reduced nucleus accumbens functional connectivity in reward network and default mode network in patients with recurrent major depressive disorder
Yudan Ding, Xiao Chen, Zuobing Chen, Le Li, Xueying Li, F. Xavier Castellanos, Tongjian Bai, Qijing Bo, Jun Cao, Zhikai Chang, Guanmao Chen, Ning-Xuan Chen, Wei Chen, Cheng Chang, Yuqi Cheng, Xilong Cui, Jia Duan, Yiru Fang, Qiyong Gong, Zhenghua Hou, Lan Hu, Li Kuang, Feng Li, Huixian Li, Kaiming Li, Tao Li, Yan‐Song Liu, Zhening Liu, Yi-Cheng Long, Bin Lü, Qinghua Luo, Huaqing Meng, Daihui Peng, Haitang Qiu, Jiang Qiu, Yuedi Shen, Yu‐Shu Shi, Tianmei Si, Yanqing Tang, Chuanyue Wang, Fei Wang, Kai Wang, Li Wang, Xiang Wang, Ying Wang, Yuwei Wang, Xiaoping Wu, Xinran Wu, Chunming Xie, Guangrong Xie, Haiyan Xie, Peng Xie, Xiufeng Xu, Hong Yang, Jian Yang, Jiashu Yao, Shuqiao Yao, Yingying Yin, Yonggui Yuan, Yu‐Feng Zang, Ai‐Xia Zhang, Hong Zhang, Ke-Rang Zhang, Lei Zhang, Zhijun Zhang, Jingping Zhao, Rubai Zhou, Yiting Zhou, Jun‐Juan Zhu, Zhi-Chen Zhu, Chao‐Jie Zou, Xi‐Nian Zuo, Chao‐Gan Yan, Wenbin Guo
Abstract
The nucleus accumbens (NAc) is considered a hub of reward processing and a growing body of evidence has suggested its crucial role in the pathophysiology of major depressive disorder (MDD). However, inconsistent results have been reported by studies on reward network-focused resting-state functional MRI (rs-fMRI). In this study, we examined functional alterations of the NAc-based reward circuits in patients with MDD via meta- and mega-analysis. First, we performed a coordinated-based meta-analysis with a new SDM-PSI method for all up-to-date rs-fMRI studies that focused on the reward circuits of patients with MDD. Then, we tested the meta-analysis results in the REST-meta-MDD database which provided anonymous rs-fMRI data from 186 recurrent MDDs and 465 healthy controls. Decreased functional connectivity (FC) within the reward system in patients with recurrent MDD was the most robust finding in this study. We also found disrupted NAc FCs in the DMN in patients with recurrent MDD compared with healthy controls. Specifically, the combination of disrupted NAc FCs within the reward network could discriminate patients with recurrent MDD from healthy controls with an optimal accuracy of 74.7%. This study confirmed the critical role of decreased FC in the reward network in the neuropathology of MDD. Disrupted inter-network connectivity between the reward network and DMN may also have contributed to the neural mechanisms of MDD. These abnormalities have potential to serve as brain-based biomarkers for individual diagnosis to differentiate patients with recurrent MDD from healthy controls.