Altered resting state dynamic functional connectivity of amygdala subregions in patients with autism spectrum disorder: A multi-site fMRI study

动态功能连接 自闭症谱系障碍 缘上回 神经科学 颞上回 心理学 静息状态功能磁共振成像 扁桃形结构 颞叶 功能连接 颞中回 功能磁共振成像 听力学 自闭症 医学 发展心理学 癫痫
作者
Yanyan Gao,Jiawei Sun,Lulu Cheng,Qihang Yang,Jing Li,Zeqi Hao,Linlin Zhan,Yuyu Shi,Mengting Li,Xize Jia,Huayun Li
出处
期刊:Journal of Affective Disorders [Elsevier BV]
卷期号:312: 69-77 被引量:13
标识
DOI:10.1016/j.jad.2022.06.011
摘要

Autism spectrum disorder (ASD) is associated with altered brain connectivity. Previous studies have focused on the static functional connectivity pattern from amygdala subregions in ASD while ignoring its dynamics. Considering that dynamic functional connectivity (dFC) can provide different perspectives, the present study aims to investigate the dFC pattern of the amygdala subregions in ASD patients. Data of 618 ASD patients and 836 typical controls (TCs) of 30 sites were obtained from the Autism Brain Imaging Data Exchange (ABIDE) database. The sliding window approach was applied to conduct seed-based dFC analysis. The seed regions were bilateral basolateral (BLA) and centromedial-superficial amygdala (CSA). A two-sample t-test was done at each site. Image-based meta-analysis (IBMA) based on the results from all sites was performed. Correlation analysis was conducted between the dFC values and the clinical scores. The ASD patients showed lower dFC between the left BLA and the bilateral inferior temporal (ITG)/left superior frontal gyrus, between the right BLA and right ITG/right thalamus/left superior temporal gyrus, and between the right CSA and middle temporal gyrus. The ASD patients showed higher dFC between the left BLA and temporal lobe/right supramarginal gyrus, between the right BLA and left calcarine gyrus, and between the left CSA and left calcarine gyrus. Correlation analysis revealed that the symptom severity was positively correlated with the dFC between the bilateral BLA and ITG in ASD. Abnormal dFC of the specific amygdala subregions may provide new insights into the pathological mechanisms of ASD.
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