Figure 1.

Proposed Network Model of Cognitive Dysfunction in Major Depressive Disorder^a

^a Abnormal recruitment and connectivity of the SN (consisting of dACC and AI), CEN (consisting of dlPFC and PPC), and DMN (consisting of PCC and vmPFC) contribute to hot (emotion dependent, indicated with dashed arrow) and cold (emotion independent, indicated with dotted arrow) cognitive dysfunction in major depressive disorder. The SN, responsible for detecting and filtering relevant information, is disproportionately affected by negative stimuli and emotional perception. The SN in major depressive disorder is also less efficient in mediating the anticorrelated activation of the CEN and DMN during cognitive tasks. Subsequent DMN overactivity results in increased negative self-referential processing and rumination that distracts from task-relevant stimuli, and the underactive CEN is less able to provide top-down inhibitory control. The net result is less efficient recruitment of networks involved in attention, working memory, and higher-order processes necessary for successful completion of cognitive tasks. SN, salience network; dACC, dorsal anterior cingulate cortex; AI, anterior insula; CEN, central executive network; dlPFC, dorsolateral prefrontal cortex; PPC, posterior parietal cortex; DMN, default mode network; PCC, posterior cingulate cortex; vmPFC, ventromedial prefrontal cortex. Adapted from Hamilton et al. (77) and Menon (74).