Mean clustering coefficients (Cp) and mean absolute path lengths (Lp) in APOE <i>ε</i>4 carriers and APOE <i>ε</i>4 noncarriers.

<p>Mean clustering coefficients (Cp) and mean absolute path lengths (Lp) in APOE <i>ε</i>4 carriers and APOE <i>ε</i>4 noncarriers.</p

A. The hub regions in APOE <i>ε</i>4 carriers (The size of the circles represents the nodal centrality in this brain region).

<p>B. The hub regions in APOE <i>ε</i>4 noncarriers. C. Differences of between-group nodal centrality in the APOE <i>ε</i>4 carriers compared with the APOE <i>ε</i>4 noncarriers. The six hub regions which are at least in a network of the APOE <i>ε</i>4 carriers and the APOE <i>ε</i>4 noncarriers and these hub regions indicate the significant between-group differences(p<0.05). The blue spheres represent nodal centrality with significant decreases and the red spheres represent nodal centrality with significant increases in the APOE <i>ε</i>4 carriers compared with the APOE <i>ε</i>4 noncarriers.</p

The FAQ scores and the average metabolism in left rolandic operculum and left superior parietal gyrus in APOE <i>ε</i>4 carriers.

<p>The FAQ scores and the average metabolism in left rolandic operculum and left superior parietal gyrus in APOE <i>ε</i>4 carriers.</p

Statistical parametric map showing a higher or lower regional cerebral metabolic rate of glucose (FDR corrected p<0.05) in APOE <i>ε</i>4 carriers compared with APOE <i>ε</i>4 noncarriers.

<p>The color bar indicates the t value. The cluster size > = 5.</p

Abnormal interregional correlations in APOE <i>ε</i>4 carriers compared with APOE <i>ε</i>4 noncarriers.

<p>The yellow dots indicate the AAL brain regions which showed the significantly abnormal correlations. The red and blue lines indicate the significantly increased and decreased interregional correlations.</p

The left image indicates the between-group differences in clustering coefficients (Cp) and the right image indicates the between-group differences in absolute path lengths (Lp).

<p>The black open circles show the average values in each property and the black lines indicate the 95% confidence intervals of the between-group differences through 1000 permutation tests in each sparsity.</p

Hub regions in metabolic networks of the APOE <i>ε</i>4 carriers and the APOE <i>ε</i>4 noncarriers listing by the descending order of the APOE <i>ε</i>4 carriers’ normalized betweenness.

<p>Hub regions in metabolic networks of the APOE <i>ε</i>4 carriers and the APOE <i>ε</i>4 noncarriers listing by the descending order of the APOE <i>ε</i>4 carriers’ normalized betweenness.</p

Topological Organization of Metabolic Brain Networks in Pre-Chemotherapy Cancer with Depression: A Resting-State PET Study

<div><p>This study aimed to investigate the metabolic brain network and its relationship with depression symptoms using ¹⁸F-fluorodeoxyglucose positron emission tomography data in 78 pre-chemotherapy cancer patients with depression and 80 matched healthy subjects. Functional and structural imbalance or disruption of brain networks frequently occur following chemotherapy in cancer patients. However, few studies have focused on the topological organization of the metabolic brain network in cancer with depression, especially those without chemotherapy. The nodal and global parameters of the metabolic brain network were computed for cancer patients and healthy subjects. Significant decreases in metabolism were found in the frontal and temporal gyri in cancer patients compared with healthy subjects. Negative correlations between depression and metabolism were found predominantly in the inferior frontal and cuneus regions, whereas positive correlations were observed in several regions, primarily including the insula, hippocampus, amygdala, and middle temporal gyri. Furthermore, a higher clustering efficiency, longer path length, and fewer hubs were found in cancer patients compared with healthy subjects. The topological organization of the whole-brain metabolic networks may be disrupted in cancer. Finally, the present findings may provide a new avenue for exploring the neurobiological mechanism, which plays a key role in lessening the depression effects in pre-chemotherapy cancer patients.</p></div

Small-world properties of the metabolic networks.

<p>Above graphs indicate the changes in the Gamma </p><p></p><p></p><p><mi>γ</mi><mo>=</mo></p><p><mi>C</mi><mi>p</mi></p><p><mi>r</mi><mi>e</mi><mi>a</mi><mi>l</mi></p><p></p><mo>/</mo><p><mi>C</mi><mi>p</mi></p><p><mi>r</mi><mi>a</mi><mi>n</mi><mi>d</mi><mi>o</mi><mi>m</mi></p><p></p><p></p><p></p><p></p> and Lambda <p></p><p></p><p><mi>λ</mi><mo>=</mo></p><p><mi>L</mi><mi>p</mi></p><p><mi>r</mi><mi>e</mi><mi>a</mi><mi>l</mi></p><p></p><mo>/</mo><p><mi>L</mi><mi>p</mi></p><p><mi>r</mi><mi>a</mi><mi>n</mi><mi>d</mi><mi>o</mi><mi>m</mi></p><p></p><p></p><p></p><p></p> in APOE <i>ε</i>4 carriers and APOE <i>ε</i>4 noncarriers (sparsity ranging from 7% to 26%).<p></p

The interregional correlations matrix in APOE <i>ε</i>4 carriers and APOE <i>ε</i>4 noncarriers.

<p>A. The correlations matrices was established by computing the partial correlations between pairs of AAL areas in every group (left: APOE <i>ε</i>4 carriers, right: APOE <i>ε</i>4 noncarriers) B:The binarized matrices drew by thresholding the partial correlations matrices of A in a sparsity threshold (7%).</p