Introduction
comorbidity, depression, late-life depression, hippocampal atrophy, LLD, WMH, disability, white matter hyperintensities
WHITE MATTER HYPERINTENSITIES
Due to cognitive changes, medical comorbidity, disability, and polypharmacy, treatment of late-life depression (LLD) is inherently complex (Taylor, Earlier work in LLD examined age-related structural brain changes, often focusing on the hippocampus or white matter hyperintensities (WMH), cerebrovascular-related structural abnormalities common in LLD. Both hippocampal atrophy and greater WMH severity has been associated with poorer antidepressant responses, although these findings are not always consistent across studies (Gunning-Dixon et al., Studies examining pre-treatment connectivity as a predictor of response in LLD are sparse and often limited by open-label trial designs or smaller sample sizes. However, they do support that variability in the antidepressant response is associated with functional connectivity differences in the CCN, salience network, reward network, and even sensorimotor regions (Alexopoulos et al., This study aimed to determine whether regional resting-state functional connectivity measures obtained prior to randomization and treatment were associated with change in depression severity over a randomized, controlled trial. We hypothesized that functional connectivity in the DMN, CCN, and limbic networks would be related to clinical improvement. Based on past work (Alexopoulos et al., 