Resting-state functional connectivity of the cerebellum-cerebrum in older women with depressive symptoms

Abstract

Abstract Background Although there has been much neurobiological research on major depressive disorder, research on the neurological function of depressive symptoms (DS) or subclinical depression is still scarce, especially in older women with DS. Objectives Resting-state functional magnetic resonance imaging (rs-fMRI) was used to compare functional connectivity (FC) between the cerebellum and cerebral in older women with DS and normal controls (NC), to explore unique changes in cerebellar FC in older women with DS. Methods In all, 16 older women with DS and 17 NC were recruited. All subjects completed rs-fMRI. The 26 sub-regions of the cerebellum divided by the AAL3 map were used as regions of interest (ROI) to analyze the difference in FC strength of cerebellar seeds from other cerebral regions between the two groups. Finally, partial correlation analysis between abnormal FC strength and Geriatric Depression Scale (GDS) score and Reminiscence Functions Scale (RFS) score in the DS group. Results Compared with NC group, the DS group showed significantly reduced FC between Crus I, II and the left frontoparietal region, and reduced FC between Crus I and the left temporal gyrus. Reduced FC between right insula (INS), right rolandic operculum (ROL), right precentral gyrus (PreCG) and the Lobule IX, X. Moreover, the negative FC between Crus I, II, Lobule IX and visual regions was reduced in the DS group. The DS group correlation analysis showed a positive correlation between the left Crus I and the right cuneus (CUN) FC and GDS. In addition, the abnormal FC strength correlated with the scores in different dimensions of the RFS, such as the negative FC between the Crus I and the left middle temporal gyrus (MTG) was positively associated with intimacy maintenance, and so on. Conclusion Older women with DS have anomalous FC between the cerebellum and several regions of the cerebrum, which may be related to the neuropathophysiological mechanism of DS in the DS group.