Amygdala network dysfunction in late-life depression phenotypes: Relationships with symptom dimensions.
Amygdala network dysfunction in late-life depression phenotypes: Relationships with symptom dimensions.
复制标题
DOI：
10.1016/j.jpsychires.2015.09.002
复制
发表时间：
2015-11
影响因子：
4.8
通讯作者：
Goveas JS
中科院分区：
文献类型：
--
作者：
Li W;Ward BD;Xie C;Jones JL;Antuono PG;Li SJ;Goveas JS
杏仁核是情绪处理神经系统的关键枢纽，与晚年抑郁症（LLD）的病理生理学有关。然而，重叠和发散的杏仁核网络功能异常是两种临床LLD表型（即，LLD单独和LLD伴轻度认知障碍[LLD-MCI]）未知。本研究的目的是调查杏仁核功能连接（FC）的差异LLD单独，LLD-MCI和健康对照，并检查杏仁核网络功能障碍和症状维度之间的关系。使用基于种子的体素R-fcMRI方法进行静息状态功能连接磁共振成像研究，以探测总共63名老年参与者（LLD [n=22]，LLD-MCI [n=15]和年龄和性别等同的健康老年人[n=26]）的杏仁核FC。与对照组相比，LLD组成年人的后默认模式和蚓部FC增加，额顶叶、显著区和颞区的连接减少。与健康对照组相比，LLD-MCI参与者在默认模式、认知控制、显著性和视觉区域中表现出FC减少，而FC增加仅限于侧顶叶皮层。LLD-MCI组还显示，相对于仅LLD组，枕部和后部默认模式区的FC减少。不同的杏仁核FC异常，解释抑郁和焦虑症状的严重程度，和执行功能被确定。杏仁核FC损伤可区分LLD表型。这些功能网络异常也可以解释LLD临床表现的异质性。
The amygdala, a crucial hub of the emotional processing neural system, has been implicated in late-life depression (LLD) pathophysiology. However, the overlapping and diverging amygdala network function abnormalities underlying two clinical LLD phenotypes (i.e., LLD alone and LLD with mild cognitive impairment [LLD-MCI]) are unknown. The aim of this study is to investigate the amygdala functional connectivity (FC) differences between LLD alone, LLD-MCI and healthy controls, and to examine the relationships between amygdala network dysfunction and symptom dimensions. A resting-state functional connectivity magnetic resonance imaging study was conducted to probe amygdala FC in a total of 63 elderly participants (LLD [n=22], LLD-MCI [n=15], and age- and gender-equated healthy older adults [n=26]) using a seed-based voxelwise R-fcMRI approach. LLD-only adults showed increased FC in the posterior default mode and vermis, and diminished connections in the fronto-parietal, salience and temporal areas, relative to controls. The LLD-MCI participants showed diminished FC in the default mode, cognitive control, salience and visual regions, whereas increased FC was limited to lateral parietal cortex compared with healthy controls. The LLD-MCI group also showed diminished FC in the occipital and posterior default mode areas, relative to the LLD-only group. Distinct amygdala FC abnormalities that explain depressive and anxiety symptom severity, and executive functioning were identified. The amygdala FC impairments may distinguish LLD phenotypes. These functional network abnormalities may also explain the heterogeneity seen in the LLD clinical presentations.