The reported lifetime prevalence of depression in adolescents has increased drastically in recent decades. Depression in this population can be particularly damaging and can frequently have a long-lasting adverse impact. The common treatment approach includes psychological therapy and/or anti-depressant medication. However, the efficacy of these approaches, both singularly and combined, is far from conclusive. Recently, there have been an increased number of studies investigating the effect of exercise and physical activity on adolescent depression, however, despite this increased attention, there are no recent reviews and meta-analyses synthesising such studies.

The review examines the treatment effect of exercise on depression symptoms for adolescents aged 13–17 years of age.

A systematic search of seven electronic databases identified relevant randomised controlled trials. Screening, data extraction and trial methodological quality were undertaken by two independent researchers. Standardized mean differences were used for pooling post-intervention depressive symptom scores.

Eleven trials met the inclusion criteria, eight of which provided the necessary data for calculation of standardized effect size. Exercise showed a statistically significant moderate overall effect on depressive symptom reduction. Sensitivity analyses were also conducted and will be presented.

Exercise and physical activity appear to improve depression symptoms in adolescents, especially in clinical samples, suggesting that exercise may be a useful treatment strategy for adolescents with depression.

Despite the positive findings, large clinical trials that adequately minimise bias are required for firmer conclusions on the effectiveness of exercise as an antidepressant treatment.

The authors have not supplied their declaration of competing interest.

Depression is considered to have the highest disability burden of all conditions. Although treatment-resistant depression (TRD) is a key contributor to that burden, there is little understanding of the best treatment approaches for it and specifically the effectiveness of available augmentation approaches.

We conducted a systematic review and meta-analysis to search and quantify the evidence of psychological and pharmacological augmentation interventions for TRD.

Participants with TRD (defined as insufficient response to at least two antidepressants) were randomised to at least one augmentation treatment in the trial. Pre-post analysis assessed treatment effectiveness, providing an effect size (ES) independent of comparator interventions.

Of 28 trials, 3 investigated psychological treatments and 25 examined pharmacological interventions. Pre-post analyses demonstrated N-methyl-d-aspartate-targeting drugs to have the highest ES (ES = 1.48, 95% CI 1.25–1.71). Other than aripiprazole (four studies, ES = 1.33, 95% CI 1.23–1.44) and lithium (three studies, ES = 1.00, 95% CI 0.81–1.20), treatments were each investigated in less than three studies. Overall, pharmacological (ES = 1.19, 95% CI 1.08–1.30) and psychological (ES = 1.43, 95% CI 0.50–2.36) therapies yielded higher ESs than pill placebo (ES = 0.78, 95% CI 0.66–0.91) and psychological control (ES = 0.94, 95% CI 0.36–1.52).

Despite being used widely in clinical practice, the evidence for augmentation treatments in TRD is sparse. Although pre-post meta-analyses are limited by the absence of direct comparison, this work finds promising evidence across treatment modalities.

In the past 3 years, A.H.Y. received honoraria for speaking from AstraZeneca, Lundbeck, Eli Lilly and Sunovion; honoraria for consulting from Allergan, Livanova and Lundbeck, Sunovion and Janssen; and research grant support from Janssen. In the past 3 years, A.J.C. received honoraria for speaking from AstraZeneca and Lundbeck; honoraria for consulting with Allergan, Janssen, Livanova, Lundbeck and Sandoz; support for conference attendance from Janssen; and research grant support from Lundbeck. B.B. has recently been (soon to be) on the speakers/advisory board for Hexal, Lilly, Lundbeck, Mundipharma, Pfizer, and Servier. No other conflicts of interest.

In bulimia nervosa (BN), borderline personality disorder (BPD) and major depression (MDD) are frequently comorbid conditions. Executive function has been found to be impaired in BPD and MDD, but the impact of comorbidity on neuropsychological function has rarely been investigated.

To investigate neuropsychological function in BN with a focus on comorbid BPD and MDD.

One hundred forty-four medication-free female patients entering a study of psychological treatments for BN performed a brief battery of neuropsychological tests. Comorbid MDD and BPD were systematically identified using standard interviews. Neuropsychological test results were compared.

Forty-one subjects had comorbid BPD and 35 had comorbid MDD, while 15 had both. There was no effect of comorbid MDD, but there was a significant effect of BPD and a significant interaction between the diagnosis of MDD and BPD on executive tasks (trail making and Stroop). Thus, compared with subjects without BPD, subjects with BPD performed significantly worse on tests of executive function, while the group with both comorbidities performed even worse.

There appears to be an additive effect of BPD and MDD resulting in impaired executive neuropsychological function. Future studies on either disorder and on BN should examine and account for the effect of comorbidity.

The anterior cingulate cortex is frequently implicated in the pathophysiology of bipolar disorder, but magnetic resonance imaging (MRI) studies have reported variable findings owing to a reliance on patient samples with chronic illness and to limited appreciation of the region's heterogeneity.

To characterise anterior cingulate cortex abnormalities in patients with bipolar disorder experiencing their first episode of psychosis while accounting for regional anatomical variability.

Grey matter volume, surface area and cortical thickness were measured in six anterior cingulate cortex subregions per hemisphere using MRI scans acquired from 26 patients with bipolar I disorder experiencing first-episode psychosis and 26 healthy controls matched for age, gender and regional morphological variability.

Relative to controls, male patients displayed increased thickness in the right subcallosal limbic anterior cingulate cortex. No significant differences were identified in females for grey matter volume or surface area measures. The findings were not attributable to medication effects.

These data suggest that first-episode psychosis in bipolar disorder is associated with a gender-specific, right-lateralised thickness increase in anterior cingulate cortex subregions known to play a role in regulating physiological stress responses.