Differentially disrupted functional connectivity of the subregions of the amygdala in Alzheimer's disease

作者:Wang, Zhiqun; Zhang, Min; Han, Ying; Song, Haiqing; Guo, Rongjuan*; Li, Kuncheng*
来源:Journal of X-Ray Science and Technology, 2016, 24(2): 329-342.
DOI:10.3233/XST-160556

摘要

The amygdala is an important brain area involved in cognitive procession and emotional regulation. Previous studies have typically considered the amygdala as a single structure, which likely masks contribution of individual amygdala subdivisions. Actually, the amygdala is heterogeneous and composed of structurally and functionally distinct nuclei, which may present different connectivity patterns and predict to relevant cognitive deficits in Alzheimer's disease (AD). However, little is known about functional connectivity of amygdala subregions in the resting state in AD subjects. Here, we employed resting-state functional MRI (fMRI) to examine functional connectivity changes of subregions comparing the AD patients with the age-matched control subjects. Thirty-two AD and 38 control subjects were analyzed. We defined three subregions of the amygdala according to probabilistic cytoarchitectonic atlases and mapped the whole-brain resting-state functional connectivity for each subregion: The central medial nucleus (CM) of amygdala exhibited connections with the lentiform nucleus, parahippocampus and lateral temporal gyrus; the lateral basal nucleus (LB) of amygdala functionally connected with the parahippocampus, lateral temporal gyrus, middle occipital gyrus and medial prefrontal cortex; and the superficial nucleus (SF) of amygdala had connection with the parahippocampus, lentiform nucleus, lateral temporal gyrus, insula, middle occipital gyrus, precentral and postcentral gyrus. Comparing with the controls, the AD patients presented disrupted connectivity patterns in the LB of amygdala, which predicted disconnection with the left uncus, right insula, right precentral gyrus, the left superior temporal gyrus and right claustrum. These findings in a large part supported our hypothesis and provided a new insight in understanding the pathophysiological mechanisms of AD.