Objective-Children of parents with depression are 2-3 times more likely to develop major depressive disorder (MDD) than those without a parental history; however, subcortical brain volume abnormalities characterizing MDD risk remain unclear. The Adolescent Brain and Cognitive Development (ABCD) Study provides an opportunity to identify subcortical differences associated with parental depressive history.Method-Structural MRI data were acquired from 9-10-year-old children (n=11,876; release 1.1=4,521; release 2.0.1=7,355). Approximately one-third of the children had a parental depressive history; providing sufficient power to test differences between low-and high-risk youth in subcortical brain volume. Children from release 1.1 were examined as a discovery sample, and we sought to replicate effects in release 2.0.1. Secondary analyses tested group differences in the prevalence of depressive disorders and clarified whether subcortical brain differences were present in youth with a lifetime depressive disorder history.Results-Parental depressive history was related to smaller right putamen volume in the discovery (release 1.1; Cohen's d=−0.10) and replication (release 2.0.1; d=−0.10) samples. However, in release 1.1, this effect was driven by maternal depressive history (d=−0.14) whereas in release 2.0.1, paternal depressive history showed a stronger relation with putamen volume (d= −0.09). Further, high-risk children exhibited a near 2-fold greater occurrence of depressive
Affect dynamics reflect individual differences in how emotional information is processed, and may provide insights into how depressive episodes develop. To extend prior studies that examined affect dynamics in currently depressed individuals, the present study tested in 68 nondepressed young adults whether three well-established risk factors for major depressive disorder (MDD) -(a) past episodes of MDD, (b) family history of MDD, and (c) reduced neurophysiological responses to reward -predicted mean levels, instability, or inertia (i.e., inflexibility) of positive affect (PA) and/or negative affect (NA). Momentary PA and NA were assessed up to 6 times per day for 14 days (mean number of surveys completed=45.89). MDD history and family history of MDD were assessed via semi-structured interview, and neurophysiological responses to reward were indexed using the Reward Positivity, an eventrelated potential related to depression. After adjusting for current depressive symptoms, results indicated that (a) past episodes of MDD predicted higher mean levels of NA, (b) family history of MDD predicted greater PA inertia, and (c) blunted reactivity to reward predicted greater NA inertia. Collectively, these results suggest that elevated mean levels of NA and inflexibility of PA and NA may be potential mechanisms that confer risk for depression.
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