Interactions between the brain networks and subnetworks are crucial for active and resting cognitive states. Whether a subnetwork can restore the adequate function of the parent network whenever a disease state affects the parent network is unclear. Investigations suggest that the control of the anterior insula-based network (AIN) over the default-mode network (DMN) and central-executive network (CEN) is decreased in individuals with mild cognitive impairment (MCI). Here, we hypothesized that the posterior insula-based network (PIN) attempts to compensate for this decrease. To test this, we compared a group of MCI and normal cognitive individuals. A dynamical causal modeling method has been employed to investigate the dynamic network controls/modulations. We used the resting state functional MRI data, and assessed the interactions of the AIN and of the PIN, respectively, over the DMN and CEN. We found that the greater control of AIN than that of DMN (Wilcoxon rank sum: Z = 1.987; p = 0.047) and CEN (Z = 3.076; p = 0.002) in normal group and the lower (impaired) control of AIN than that of CEN (Z = 8.602; p = 7.816 × 10-18). We further revealed that the PIN control was significantly higher than that of DMN (Z = 6.608; p = 3.888 × 10-11) and CEN (Z = 6.429; p = 1.278 × 10-10) in MCI group where the AIN was impaired, but that control was significantly lower than of DMN (Z = 5.285; p = 1.254 × 10-7) and CEN (Z = 5.404; p = 6.513 × 10-8) in normal group. Finally, the global cognitive test score assessed using Montreal cognitive assessment and the network modulations were correlated (Spearman’s correlation: r = 0.47; p = 3.76 × 10-5 and r = -0.43; p = 1.97 × 10-4). These findings might suggest the flexible functional profiles of AIN and PIN in normal aging and MCI.

Hypertensive African-Americans have a greater risk of cognitive impairment than hypertensive Caucasian-Americans. The neural basis of this increased risk is yet unknown. Neuroimaging investigations suggest that the normal neural activity comprises complex interactions between brain networks. Recent studies consistently demonstrate that the insula, part of the salience network, provides modulation effects (information flow) over the default-mode and central-executive networks in cognitively normal subjects, and argue that the modulation effect is declined in cognitive impairment. The purpose of this study is to examine the information flow at the nodes of three networks using resting state functional magnetic resonance imaging (MRI) data in cognitively impaired hypertensive individuals with the African-Americans and the Caucasian-Americans races, and to compare the thickness of impaired node between two racial groups. Granger causality methodology was used to calculate information flow between networks using resting state functional MRI data, and FreeSurfer was used to measure cortical thickness from T1-weighted structural images. We found that negative information flow of the insula in both African-Americans and Caucasian-Americans, which was in contrast with previously reported positive information flow in this region of normal individuals. Also, significantly greater negative information flow in insula was found in African-Americans than Caucasian-Americans (Wilcoxon rank sum; Z = 2.06; p < 0.05). Significantly, lower insula thickness was found in African-Americans compared with Caucasian-Americans (median = 2.797 mm vs. 2.897 mm) (Wilcoxon rank sum; Z = 2.09; p < 0.05). Finally, the insula thickness correlated with the global cognitive testing measured by Montreal cognitive assessment (Spearman's correlation; r = 0.30; p < 0.05). These findings suggest that the insula is a potential biomarker for the racial disparity in cognitive impairment of hypertensive individuals.