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• Adolescents with depression were marginally faster than those in the comparison group to recognise sadness, although this trend disappeared once covarying for age and use of antidepressant medication. • Within the depression group, severity of depression symptoms and borderline personality features were associated with poorer emotional facial expression recognition (EFER) performance. • Discrepancies between group and within-group differences may explain some of the clinical heterogeneity observed in studies of EFER amongst adolescents with depression. • Studying clinical features in relation to EFER in adolescents with depression allows for a more nuanced understanding of social difficulties that may be experienced in depression. Studies have reported that emotional facial expression recognition (EFER) may be altered in individuals with depression. This study examined EFER in adolescent girls with and without depression and further examined associations between relevant clinical features of depression and EFER. Fifty adolescent girls aged 12 to 19 years old meeting criteria for depression or subthreshold levels of symptomatology and 55 adolescent girls with no psychiatric diagnosis completed EFER tasks. Reaction time and accuracy for recognising expressions at high and low intensities, and sensitivity in recognising happiness, sadness, anger and fear were assessed. Data were analysed using linear mixed models. Adolescents with depression were marginally faster than those in the comparison group to recognize sadness, although this trend disappeared once covarying for age and antidepressant use. Amongst adolescents with depression, clinical features were associated with poorer EFER performance. In contrast, anxiety symptoms were linked to better accuracy and heightened sensitivity towards happiness. A better understanding of EFER in adolescent girls with and without depression, and how clinical features might be associated with altered patterns of EFER could help to explain clinical heterogeneity observed in such studies of adolescents with depression. Knowledge of socio-cognitive alterations associated with depression will help to better develop and tailor interventions. [ABSTRACT FROM AUTHOR]

Depression is associated with alterations in hypothalamic–pituitary–adrenal (HPA) axis activity. A proposed mechanism to explain these alterations are changes in DNA methylation levels, secondary to early life adversity (ELA), at stress-related genes. Two gene regions that have been implicated in the literature, the glucocorticoid receptor gene ( NR3C1 ) exon 1F and the FKBP5 gene intron 7 were examined in 67 individuals (33 depressed patients and 34 controls). We investigated whether cortisol concentrations, evaluated in 25 depressed patients and 20 controls, and measures of ELA were associated with the degree of methylation at these candidate gene regions. Mean NR3C1 exon 1F DNA methylation levels were significantly increased in the depressed cohort and the degree of methylation was found to be positively associated with morning cortisol concentrations. DNA methylation levels at specific CG sites within the NR3C1 exon 1F were related to childhood emotional abuse severity. DNA methylation at CG38 was related to both HPA axis and childhood emotional abuse measures in the depressed group. No FKBP5 differences were revealed. Our findings suggest that hypermethylation at the NR3C1 exon 1F may occur in depression. This locus-specific epigenetic change is associated with higher basal HPA axis activity, possibly reflecting acquired glucocorticoid receptor resistance. [ABSTRACT FROM AUTHOR]