Current maternal depression moderates the relation between critical expressed emotion in mothers and depressive symptoms in their adolescent daughters

a b s t r a c t Prior studies have examined critical expressed emotion (EE-Crit) in mothers in the intergenerational transmission of depression. However, the potential moderating effect of maternal depression diagnostic status in relation to EE-Crit and youth depressive symptoms has yet to be determined. A total of N¼ 121 biological mother/daughter dyads that differed in maternal depression diagnostic status were recruited for the present study: (1) currently depressed mothers (current depression, n ¼29); (2) formerly depressed mothers (past depression, n ¼39); and (3) mothers free from any psychiatric history (healthy controls, n ¼53). Mothers were administered structured clinical interviews and completed self-report measures of EE-Crit and psychopathology, and daughters self-reported depressive symptoms. Results indicated no significant group differences in EE-Crit; however, current maternal depression status moderated EE-Crit such that the magnitude of the relation between EE-Crit and adolescent depressive symptoms was significantly greater in daughters of currently depressed mothers. These findings highlight the importance of considering current maternal depression, rather than a history of maternal depression, in relation to EE-Crit and adolescent depressive symptoms, providing impetus for future investigations

Neural Response to Peer Rejection in Clinically Depressed Adolescents and Healthy Controls

Major depression is a debilitating and highly recurrent mental illness that typically emerges during adolescence (Hankin, 2006). The increased vulnerability to depression observed during adolescence is posited to arise in part from major neurobiological changes that occur during typical development (Davey, Yücel, & Allen, 2008). Importantly, these neurobiological changes occur while the adolescent’s focus shifts from parents to peers (Steinberg, 2005). Social reward (e.g., peer acceptance) is therefore thought to be particularly salient, and a failure to obtain social reward (e.g., through social rejection) has been implicated as a driving force in the vulnerability to and maintenance of adolescent depression (Davey et al., 2008; Mellick, Sharp, & Ernst, 2015). Indeed, social rejection during adolescence is highly predictive of depression (Prinstein & Aikens, 2004), and currently depressed adolescents experience more rejection than their healthy peers (Lee, Hankin, & Mermelstein, 2010). Several adult and youth depression studies have examined response to social rejection revealing greater distress among depressed individuals; however, these studies relied predominantly on self-report or behavioral data. Therefore, the neurobiological underpinnings of rejection in depression remain underexplored despite the fact that such findings may inform etiological and theoretical models of depression, helping to further classify depression in terms of neural circuitry. Against this background, a total of N = 35 adolescents were recruited to form two groups (Depressed, n = 17; Healthy controls, n = 18) who experienced rejection during fMRI scanning. This study had two aims: 1) To compare neural response to peer rejection in depressed adolescents versus healthy controls, and 2) To examine sex as a moderator of the relation between depression and neural response to rejection. Whole-brain voxel-wise and region of interest (ROI) between-group analyses were performed. Whole-brain results showed depressed adolescents to exhibit significantly greater rejection response in the right anterior insula, left occipital operculum, and left nucleus accumbens. Reduced ventral striatal response to social inclusion was not found in depressed adolescents. ROI analyses led to null findings with no significant differences observed between groups. Insufficient samples sizes prohibited examining sex as a moderator. Exploratory tests of pubertal x group effects were conducted though non-significant, which was presumably due to limited data. Positive and null results are discussed in relation to extant neuroimaging findings in healthy and depressed samples with an emphasis on discrepancies across studies which may be due to methodological differences. The present study was among the few to recently employ Cyberball in the study of psychiatric populations marked by interpersonal functioning deficits and contributes to the identification of unique and/or shared neural substrates of an important interpersonal process in adolescent depression.Psychology, Department o

The Relation Between Adolescent Depression and Interpersonal Trust

Depression has been conceptualized as a highly interpersonal illness. In the study of social cognition, behavioral economic games (or games of social exchange) provide a novel means to examine interpersonal relations in individuals with psychological disorder. Recently, there have been several behavioral economic studies of adult depression, and the current study downwardly extends this investigative approach to adolescent depression. N = 76 age-matched adolescent girls (depressed inpatients, n = 38; healthy controls, n = 38) played a modified version of the trust game to examine the prospective relations between adolescent depression and interpersonal trust. Depressed girls were found to make significantly larger mean investments in the trust game, as compared to healthy controls. This relation between depression and excessive trust was similarly found using another measure of depression by which the total sample was divided into groups based on severity of depressive symptoms. Severely depressed girls made significantly larger mean investments in the trust game, as compared to minimally depressed girls. Linear regression analyses revealed dimensional scores from the YSR affective problems scale to be a significant predictor of trust game performance. While further replication is needed, these preliminary findings suggest that adolescent depression may be characterized by excessive trust.Psychology, Department o

Identification of genetic modifiers of age-at-onset for familial Parkinson’s disease

Parkinson’s disease (PD) is the most common cause of neurodegenerative movement disorder and the second most common cause of dementia. Genes are thought to have a stronger effect on age-at-onset of PD than on risk, yet there has been a phenomenal success in identifying risk loci but not age-at-onset modifiers. We conducted a genome-wide study for age-at-onset. We analysed familial and non-familial PD separately, per prior evidence for strong genetic effect on age-at-onset in familial PD. GWAS was conducted in 431 unrelated PD individuals with at least one affected relative (familial PD) and 1544 non-familial PD from the NeuroGenetics Research Consortium (NGRC); an additional 737 familial PD and 2363 non-familial PD were used for replication. In familial PD, two signals were detected and replicated robustly: one mapped to LHFPL2 on 5q14.1 (PNGRC = 3E-8, PReplication = 2E-5, PNGRC + Replication = 1E-11), the second mapped to TPM1 on 15q22.2 (PNGRC = 8E-9, PReplication = 2E-4, PNGRC + Replication = 9E-11). The variants that were associated with accelerated onset had low frequencies (<0.02). The LHFPL2 variant was associated with earlier onset by 12.33 [95% CI: 6.2; 18.45] years in NGRC, 8.03 [2.95; 13.11] years in replication, and 9.79 [5.88; 13.70] years in the combined data. The TPM1 variant was associated with earlier onset by 15.30 [8.10; 22.49] years in NGRC, 9.29 [1.79; 16.79] years in replication, and 12.42 [7.23; 17.61] years in the combined data. Neither LHFPL2 nor TPM1 was associated with age-at-onset in non-familial PD. LHFPL2 (function unknown) is overexpressed in brain tumours. TPM1 encodes a highly conserved protein that regulates muscle contraction, and is a tumour-suppressor gene